Whoa!!!!
The level of complexity within the cell has just gone up ANOTHER step.
Here the language is immensely informative: Codes, Hidden Codes, Decyphering of a code, translation, synonymous codes. I can go on and on. Clearly these codes and decoding are not somethings that can happen by chance since there is no materialistic way to create a code and its decoding counterpart. There just is none.

The only way codes and their decoding measures can arise is through intelligence. They are completely independent of the materialistic implementation. AND THEY ARE ABSTRACT.

*sigh* scientists need to stop using metaphors (genetic "code"), or misinformed fanatics will keep spewing their garbage.

kevinrtrs, please read a book, m'kay?

there is no materialistic way to create a code and its decoding counterpart. There just is none.

You mean no way that YOU can see.
First because you don't bother to understand what scientists mean by 'codes' (hint - it's not cloak and dagger spy versus spy stuff).
Second because you don't understand how variation and natural selection work over time to accumulate complexity.
And third because you only think in terms of 6000 years.

Evolution has created many 'codes', such as RNA and DNA, histone tagging, intra-cellular signalling cascades, inter-cellular signalling, timing encoded neuron firing, etc.
These codes are not created as complete codes, but evolve bit by bit from simpler signalling and feedback loops.

When variation and natural selection are programed in computers, they come up with amazingly powerful algorithms in just thousands of generations, and nature has had millions and even billions of generations.

Try taking your young-earth blinders off for a change.

Whoa!!!!
The level of complexity within the cell has just gone up ANOTHER step.
Here the language is immensely informative: Codes, Hidden Codes, Decyphering of a code, translation, synonymous codes. I can go on and on. Clearly these codes and decoding are not somethings that can happen by chance since there is no materialistic way to create a code and its decoding counterpart. There just is none.

The only way codes and their decoding measures can arise is through intelligence. They are completely independent of the materialistic implementation. AND THEY ARE ABSTRACT.

Do your job, moderators.

A hidden genetic code altered only by nutrients could not lead to beneficial adaptations via mutations, which are typically deleterious. Instead, species diversification is controlled by the metabolism of nutrients to pheromones.

The epigenetic effects of nutrient chemical stress and social stress alter the microRNA/messenger RNA balance, intracellular signaling, and stochastic gene expression that is responsible for adaptive evolution. That's how chemical ecology is linked to the cellular metabolism of nutrients that chemically control reproduction. As indicated, the systems biology approach is the same in all organisms.

Nutrient-dependent pheromone-controlled reproduction of E. coli via quorum sensing ensures that the organism does not exhaust its nutrient supply. In this article, however, nutrient-dependent perturbations are inappropriately placed in the context of mutating codons instead of pheromone-controlled chromatin remodeling and social stressors.

Contrary to human-like intelligence, evolution has no drive to keep things simple or tidy. Variations in codon efficiency are subject to selection just like any other trait, and thus are likely to have some effect. "Complexity" is the expected result of evolutionary processes. Stupid creationists dont realise that discoveries such as this speak in favor of evolution, if anything.

Look at some designs evolutionary algorithms come up with in engineering. They often appear much more complex than anything a human designer can come up with.

Variations in codon efficiency are subject to selection just like any other trait, and thus are likely to have some effect.

Are you able to address these variations in terms of cause and effect that somehow enables adaptive evolution? What effect is selected for, and how?

Reproductive isolation evidently can arise with little or no morphological differentiation (Dobzhansky 1972). Do you think that fact presents a problem to theorists who refuse to clearly state what's naturally selected or sexually selected? Do you think it makes them appear to be fools when they state that selection is for mutations / "variations in codon efficiency"?

In your case, are you simply pitting your belief in inexplicable "variations" against the fact that the variations are nutrient-dependent and pheromone-controlled -- as exemplified in every species on the planet?

If so, your belief does not incorporate any human-like intelligence. "Nutrient-dependent pheromone-controlled" variation does.

@JVK - lack of morphological differentiation does not imply lack of differentiation.
What is selected for has been stated many times: reproductive success (typically through individual selection with an admixture of kin selection).

Why do you say that the variations are inexplicable? Many causes of mutations are known, and mutation rates have been measured in numerous species (including humans).

Why do you think that nutrient-dependent pheromone-controlled variation would require human-like intelligence? If it is beneficial it will be selected for through kin selection.
(And if an intelligence designed it, why would it have allowed 'cheaters' as have been found in so many cases of cooperation?)

RealScience eludes mention of how mutations cause adaptive evolution and regurgitates the nonsensical theory that they somehow do cause something that's important for reproductive success. Given the fact that nutrients are essential to reproduction that is controlled by pheromones in species from microbes to man, let's compare theory to fact. In theory, mutations somehow cause something that's adaptive. In fact, nutrients are selected and metabolized to species-specific pheromones that control reproduction. Is there really a need for speculation about how much intelligence is required to Create living systems that not only are epigenetically controlled by chemical ecology but also epigenetically control their species survival? What's required is for one of the theorists to explain how mutations/variations cause adaptive evolution via reproductive success or anything else. I've never seen a theorist even attempt to do so in the context of biological facts.

@JVK - mutations alone don't cause adaptive evolution. Mutations plus selection do.
This has been verified in bacteria where most mutations are harmful or neutral, but some mutations provide antibiotic resistance, which is useful when antibiotics are present (whether from natural source such as soil fungi or introduced by humans. So not only can and have theorists described it, but experimentalist have repeatedly observed it.

As a medical laboratory scientist with considerable expertise in microbiology, I should say only that it is obvious you do not know what you are talking about. I will add, however, that you have now failed to indicate how selection for mutating codons that convey antibiotic resistance occurs.

This gives you yet another opportunity to tell others HOW mutations CAUSE selection so we can compare your ridiculously vague version of cause and effect to detailed explanations of the molecular mechanisms that are required (e.g., in the context of biological facts.) If you're not going to include any biological facts, you can make up any story you wish, and claim that the theorists have described something that they've also observed.

The beauty of theory is that no biological facts are ever required; it's all so automagical, isn't it? For contrast see: http://dx.doi.org...i0.17338

Also for contrast see the article from New Scientist magazine [subscription required] Genes from nowhere: Orphans with a surprising story http://www.newsci...ry.html? "...protein-making factories in yeast are constantly churning out new proteins, allowing them to be "tested".... Carvunis thinks there is a whole continuum of "proto-genes". Most will code for proteins that are neutral or harmful, so there will be no selection and the vast majority of proto-genes will revert to non-coding DNA sooner or later. But a few proto-genes that are neutral or maybe even helpful will sometimes persist, and start to gather beneficial mutations. Over millions of years of natural selection, they can become a proper gene - and thus is an orphan born."

Natural selection for what? No evidence suggests mutations cause adaptive evolution. All evidence suggests that nutrient chemicals and pheromones epigenetically cause it!

you have now failed to indicate how selection for mutating codons that convey antibiotic resistance occurs... it is obvious you do not know what you are talking about ... For contrast see: http://dx.doi.org...i0.17338

@JVK - What got your panties in a bunch? It is silly to contrast the completeness of a <1000 character comment with a paper 30 times as long.
But if you really think that phys.org readers won't know something so basic:
Bacteria with mutated codons that convey antibiotic resistance (typically through faster pumping out of the antibiotic) survive better when exposed to antibiotics, and are thus 'selected' by the antibiotic to pass on their genes.

Rather than critiquing others, why don't YOU rebut kevinrtrs in 1000 characters? Convince him that olfaction has an evolutionary trail from unicellular organisms to insects to humans, for example, by going into detailed explanations of the molecular mechanisms.

@JVK - by the way, I happen to agree that humans sense pheromones and that the older medical thinking that they don't is flawed.

But that doesn't mean that nutrient-and-pheromone driven epigenetic changes are the ONLY thing involved in natural selection.

Rather than critiquing others, why don't YOU rebut kevinrtrs in 1000 characters?

He correctly attested to the complexity of the systems biology, which I alluded to as: "The epigenetic effects of nutrient chemical stress and social stress alter the microRNA/messenger RNA balance, intracellular signaling, and stochastic gene expression that is responsible for adaptive evolution.

If someone explains to him how mutations cause adaptive evolution, I'll be happy to explain why they can't.

But that doesn't mean that nutrient-and-pheromone driven epigenetic changes are the ONLY thing involved in natural selection.

I get that a lot. Usually it's tactical. I say that the epigenetic effects of nutrients and pheromones cause adaptive evolution -- and the come back is "That's not all there is to it." -- or as you indicated not the ONLY thing involved in natural selection.

I'm asking you how mutations cause adaptive evolution and about what is being selected. You continue to fail to indicate how selection for mutating codons that convey antibiotic resistance occurs...

Next we could attempt to discuss the respective roles of mutations, nutrients, and pheromones in ecological, social, neurogenic, and socio-cognitive niche construction. But first, tell me what it is that you think mutations cause and how they cause it.

You continue to fail to indicate how selection for mutating codons that convey antibiotic resistance occurs...

Did you miss this?

Bacteria with mutated codons that convey antibiotic resistance (typically through faster pumping out of the antibiotic) survive better when exposed to antibiotics, and are thus 'selected' by the antibiotic to pass on their genes.

Most SNP mutations cause only a mild change in the rate of a protein's expression in nutrient-poor conditions. Most of the rest cause a change far from the active site that merely shifts the intervening electrons slightly, and slightly changes the binding of the protein, and the rest of the connectome compensates. A few mutations change what the active site binds to, through changing the folding or charge density. A few of these are fatal (e.g., Huntington's).
And those are the small mutations involving proteins - SNPs can also affect regulating RNAs, and there are also bigger mutations.

Why do you ask?

Oh, I agree that biology is complex, and that science is just scratching the surface. In fact it is more more complex than just pheromones, nutrients and epigenetics. (Don't worry, there being more than pheromones won't interfere with your pheromone business or book sales).

If someone explains to him how mutations cause adaptive evolution, I'll be happy to explain why they can't.

I have explained that mutations provide the variety needed for adaptive evolution, and that natural selection accumulates useful changes from that variation, and given antibiotic resistance as an example.
So be happy and explain why they can't.

Don't bother trying to get him to understand what the other 99.9999% of biologists already understand. Pheromone-directed post-transcriptional evolution is his pet theory because he's on the payroll of human pheromone companies. His papers are just as convoluted and meaningless as his posts here.

If your hypothesis had any ground to stand on, you'd be trying to convince people in academia rather than spouting it over and over on some random science website, JVK.

This is of course nothing new, the canonical code doesn't even code for all proteogenic AAs [ http://en.wikiped...ino_acid ].

It is a mess, and it is another test for evolution that produces such - the messier, the more we understand what is going on. =D

Speaking of which, creationists shouldn't comment on science. It is hilarious, and it makes deconverts from religion, see Dawkins's Convert's Corner.

Our rude resident creationist troll has most likely made more atheists than his peers. Whoa!!!

@neversaidit: The troll can't read books, because they are coded in evolved languages. Which by themselves shows that his YEC fantasies are wrong, their evolution took more time than his decrepit invisible bearded men wet fantasies can imagine.

@aroc: :-)

His papers are just as convoluted and meaningless as his posts here.

If your hypothesis had any ground to stand on, you'd be trying to convince people in academia rather than spouting it over and over on some random science website, JVK.

People in academia already are convinced. I'm here because this is where I find the most ignorance years after winning awards for publication in peer reviewed journals.

Human pheromones: integrating neuroendocrinology and ethology Zdenek Klein award: http://www.ncbi.n...11600881

The Mind's Eyes: Human pheromones, neuroscience, and male sexual preferences. Reiss Theory Award http://www2.hu-be...kohl.htm

When someone says these papers are convoluted and meaningless they betray their own ignorance. Thanks to the anonymous "aroc91" for doing that... again.

Speaking of which, creationists shouldn't comment on science. It is hilarious, and it makes deconverts from religion, see Dawkins's Convert's Corner.

Dawkins et. al., seem to have missed the fact that no evidence suggests mutations cause adaptive evolution. Instead, there is evidence that all cytochrome P450 (CYP)genes today arose from a single ancestor, which originated probably more than 3 billion years ago. The apparent 'increased responsiveness' in mammals to diet, pheromones, chemical inducers, and drugs of three of these gene families attests to epigenetic cause (i.e., nutrients) and epigenetically controlled reproduction (e.g. by pheromones).

The obviousness of epigenetic cause in the context of nutrient dependent pheromone-controlled adaptive evolution in species from microbes to man is what makes Dawkins and others like him seem to be even more foolish than they were before the molecular mechanisms of cause and effect were detailed. Doesn't it?

If you say so. I'll admit you're right when you single-handedly topple the mutation selection hypothesis that you claim has no bearing in reality.

http://www.ncbi.n...15101972

"People in academia are already convinced"

Which is why I've never heard your model mentioned and why the mutation selection throughout my years of schooling, right?

http://www.lehigh...aper.pdf

Stupid comment box deleting text while I'm editing.

Which is why I've never heard your model mentioned and why *I've been taught* the mutation selection model throughout my years of schooling, right?

Which is why I've never heard your model mentioned and why *I've been taught* the mutation selection model throughout my years of schooling, right?

You've been taught what your professors learned, and you accepted their ignorance without challenge as demonstrated here in your challenges to me. No one told you how random mutations caused adaptive evolution, but you bought into it because it fit your intellectual grasp.

Time to learn something new: http://medicalxpr...nts.html

Watch the video; realize the complexity of receptor-mediated intracellular signaling and stochastic gene expression that led to adaptive evolution of the 5-6 million switches in the human genome starting with microbes and glucose uptake, with reproduction controlled by nutrient-dependent pheromone production.

Mutations "theory" is nothing more than an idiot's view of the basic principles of biology. Look up 'de novo' gene expression.

Mutations "theory" is nothing more than an idiot's view of the basic principles of biology.

99.99% of academia are idiots then? I learned something today.

Question: You say that selection is dependent on "preexisting genetic diversity" rather than diversity dependent on mutation. What is the source of that diversity, then?

...that led to adaptive evolution of the 5-6 million switches in the human genome...

So were all those switches already there, ready to function, in the ancestral microbes?
If you think so, then point to one microbe today with that many switches.
If not, then how did they get there?
Maybe mutations (including gene duplications and then codon changes that were beneficial because then allowed one of the duplicates to become a new switch)?
If you don't agree that mutations CONTRIBUTED to the evolution of the 5-6 million switches, then document your proposed mechanism down to "detailed explanations of the molecular mechanisms".

Inform yourselves. I'm not here to teach you what you would have learned if you had ever questioned the ridiculous theory about mutations.

'Genes from nowhere: Orphans with a surprising story" -- is in the current issue of New Scientist, which is not great science, but much better than the BS theory you were taught to believe in.

De novo gene expression is obviously nutrient chemical-dependent -- as is life in all organisms. The metabolism of nutrients to species-specific pheromones controls reproduction in species from microbes to man (as best exemplified in the honeybee model organism).

I've published a book; a series of papers; and a book chapter on this. The latest presentation of the model is here: http://f1000.com/.../1092760

Neither of you have a clue as to how ignorant you actually are, do you? What was the last review article you read that described how random mutations caused anything that was adaptive? Is there a model for that?

Neither of you have a clue as to how ignorant you actually are, do you? What was the last review article you read that described how random mutations caused anything that was adaptive? Is there a model for that?

Ignoring the links I posted on the first page, huh?

Neither of you have a clue as to how ignorant you actually are, do you? What was the last review article you read that described how random mutations caused anything that was adaptive? Is there a model for that?

Ignoring the links I posted on the first page, huh?

No. Your ongoing ignorance now forces me to note that the 2004 abstract states: "This model has successfully predicted mutation frequencies in genes of E. coli and humans." That says nothing about HOW mutation frequencies CAUSE adaptive evolution, which is obviously nutrient-dependent and pheromone-controlled in my model, which you are ignoring.

Ignoring the links I posted on the first page, huh?

Again, NO. Behe writes: "Adaptive evolution can cause a species to gain, lose, or modify a function. Therefore, it is of basic interest to determine whether any of these modes dominates the evolutionary process under particular circumstances. The results of decades of experimental laboratory evolution studies strongly suggest that, at the molecular level, loss-of-FCT and diminishing modification-of-function adaptive mutations predominate."

The mutations now somehow become adaptive at the molecular level. How do organisms select for mutations that are somehow adaptive at the molecular level. Is there a model for that? If not, aren't you simply regurgitating ridiculous theory and citing works that never made sense in the first place? It's not possible to compare them to anything that does make biological sense, like nutrient-dependent pheromone-controlled species diversification.

You're not very bright, are you?

"...eye reduction is not simply caused by accumulation of selectively neutral mutations, but must be subject to selection"

http://rsbl.royal...l?cpetoc

Selection for WHAT? What was inferred about the ignorance of 99.9% of whatever they're called? Can they really be that ignorant?

Diet Shaped Dog Domestication by Elizabeth Pennisi on 23 January 2013, 1:17 PM
http://news.scien...l?ref=hp

Excerpt: "…dogs have evolved to eat a more varied diet than their wolf ancestors. The shift parallels genetic changes seen in people and bolsters the idea that dogs and humans share similar evolutionary stories."

That's enlightening, isn't it. Diet driven changes in the behavior of subspecies... who else has modeled that -- in species from microbes to man, for example -- as I did.

http://dx.doi.org...i0.17338

Let me reiterate this: Mutations "theory" is nothing more than an idiot's view of the basic principles of biology.

http://www.pnas.o...228.full

Just four idiots regurgitating what they were taught, then?

http://www.pnas.org/content/103/30/11228.full
Just four idiots regurgitating what they were taught, then?

No. One idiot, you! You seem to think that the mere mention of the word mutation infers cause because that's what you were taught to think. And you've shown us all that you are not capable of independent thought. You can't even find anything more recent than a 2006 journal article for comparison to my award-winning 2006 journal article/book chapter in the Handbook of the Evolution of Human Sexuality. Do others understand how pitifully ignorant of biology you are? Did you look up "de novo" gene expression?

Did you look up "de novo" gene expression?

http://www.scienc...abstract

Excerpt: "In parallel to 5hmC conversion, repression of the de novo (Dnmt3a/b) and maintenance (Uhrf1) DNA methylation systems...."

In discussion of transgenerational epigenetic inheritance (above), I wonder why anyone would believe mutations led to sexual reproduction without ever being told how they could do that. For contrast, would anyone not believe that reproduction is nutrient-dependent and pheromone-controlled in species from microbes to man? Simply put, it all comes down to sense vs. nonsense. Mutations theory has always been nonsense. Nutrient-dependent pheromone-controlled adaptive evolution has always made sense.

see also: http://rstb.royal...abstract

and my most recent published work:

http://dx.doi.org...i0.17338

Part of being a good scientist is humility and the ability to explain yourself properly. All you ever do is repeat the same thing and swat away anything that seems to contradict you without actually explaining what's wrong with it.

Secondly, we found rearrangements within the central tandem repeat domain of the coding region that yield a more hydrophobic Flo11p variant. Together, these mutations result in dramatic increase in cell surface hydrophobicity, which in turn confers these yeasts the ability to float by surface tension

What, exactly, is wrong with this conclusion? Explain it. Don't just cite yourself and call me an idiot again.

They saw that specific genotype mutation and the phenotype that it resulted in. What is wrong with that?

I'm not denying the involvement of epigenetics and nutrient/pheromone post-transcriptional modification. I'm just wondering how you can throw these results out without a reasonable explanation.

@JVK You are the one who is repeating without acknowledging answers or overcoming objections. For example you repeat:

How do organisms select for mutations that are somehow adaptive at the molecular level. Is there a model for that?

I'll repeat the answer using simpler words:
Organisms DON'T select mutations. Mutations happen, and organisms try to deal with the consequences.
Mutations are selected within GROUPS of organisms by the rate at which organisms with given sets of mutations reproduce relative to organisms with other sets of mutations.
You have REPEATEDLY ignored the difference, so it looks like you do not even understand even the basics of the theory that you are disputing.

And you STILL haven't answered where the variety of genes COMES FROM without mutation. Did our unicellular ancestors have ALL of the genes that we do? If so, provide evidence. If not, then explain how the new genes arose if you say that it was not mutation.

[q And you STILL haven't answered where the variety of genes COMES FROM without mutation. Did our unicellular ancestors have ALL of the genes that we do? If so, provide evidence. If not, then explain how the new genes arose if you say that it was not mutation.

I've asked you to search on "de novo gene expression" which answers your questions above, which I have already answered by simply saying that adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man, while supporting that statement with a recently published journal article. You continue with the ridiculous claim that mutations cause something adaptive, and there has never been any scientific evidence for mutation-driven selection/speciation.

Must I end my participation here to avoid any further nonsense? Or will you attempt to learn something about biology?

You continue with the ridiculous claim that mutations cause something adaptive, and there has never been any scientific evidence for mutation-driven selection/speciation.

Ignoring what I posted. Imagine that.

Secondly, we found rearrangements within the central tandem repeat domain of the coding region that yield a more hydrophobic Flo11p variant. Together, these mutations result in dramatic increase in cell surface hydrophobicity, which in turn confers these yeasts the ability to float by surface tension

Part of being a good scientist is humility and the ability to explain yourself properly. All you ever do is repeat the same thing and swat away anything that seems to contradict you without actually explaining what's wrong with it.

We're not discussing science. You're challenging me on my well-detailed model (and a series of published works), with no evidence to support your ridiculous theory of mutational cause. If we were discussing science, we would be discussing my model.

I'm not denying the involvement of epigenetics and nutrient/pheromone post-transcriptional modification. I'm just wondering how you can throw these results out without a reasonable explanation.

What reasonable explanation is that? Random mutations? Mutations? Where is the evidence to support anything that you think can be compared to details of nutrient-dependent pheromone-controlled adaptive evolution in species from microbes to man? I'm throwing out your garbage theory, nothing more.

You continue with the ridiculous claim that mutations cause something adaptive, and there has never been any scientific evidence for mutation-driven selection/speciation.

Ignoring what I posted. Imagine that.

Secondly, we found rearrangements within the central tandem repeat domain of the coding region that yield a more hydrophobic Flo11p variant. Together, these mutations result in dramatic increase in cell surface hydrophobicity, which in turn confers these yeasts the ability to float by surface tension

Are you saying the mutations caused the floating yeast to adaptively evolve and become humans? If not, what does the floating have to do with anything in the context of nutrient-dependent pheromone-controlled adaptive evolution? I wouldn't ignore anything if you clarify what you think about cause and effect. You're simply tossing up more nonsense.

@JVK De novo gene expression deals with when the genes are EXPRESSED. I have not argued against expression being epigenetically controlled, and nutrients are well known to be factors in that (and no doubt pheromones are as well). Nor have I seen either of us argue against your catch phrase of "nutrient-dependent pheromone-controlled" effects being IMPORTANT.
(And I haven't seen aroc91 argue against that either.)

But YOU appear to believe that MUTATIONS HAVE NO ROLE in evolution, and that the only factor is your catch-phrase. Yet you STILL haven't answered where the huge variety of genes themselves comes from in your model.

Do you maintain that all present genes of all multicellular creatures, in all their variety, were in the their multicellular ancestors? If not, then explain the variety genes present today.

@JVK - by the way, calling people "idiots" doesn't count as answering.

@JVK - by the way, calling people "idiots" doesn't count as answering.

It's the only way to answer idiots. Asking whether I "... maintain that all present genes of all multicellular creatures, in all their variety, were in their multicellular ancestors, or for me to explain the variety of genes present today, qualifies you as an idiot -- one who seems to believe that mutations are causal despite the clarity of my model.

If I were to detail the role of the microRNA / messenger RNA balance that is responsible for the epigenetic landscape becoming the physical landscape via chromatin remodeling, it would make no difference, would it? You would still be an idiot who believes that mutations cause adaptive evolution.

Are you saying the mutations caused the floating yeast to adaptively evolve and become humans? If not, what does the floating have to do with anything in the context of nutrient-dependent pheromone-controlled adaptive evolution? I wouldn't ignore anything if you clarify what you think about cause and effect. You're simply tossing up more nonsense.

The mutation in the coding region incidentally made the surface protein more hydrophobic, resulting in an increased propensity to float, exposing the yeast to more oxygen. How is that nonsense?

Mutations don't _cause_ adaptive evolution. Environmental pressures resulting in selection do. If a strain of yeast doesn't get as much oxygen as another, obviously it's not going to grow as well.

Mutations don't _cause_ adaptive evolution. Environmental pressures resulting in selection do. If a strain of yeast doesn't get as much oxygen as another, obviously it's not going to grow as well.

In my model, if a strain of yeast doesn't eat, it dies. If it eats too much and exhausts its food supply it dies. Pheromones control reproduction via quorum-sensing, which helps to ensure the food supply is not exhausted.

For contrast, in your ridiculous theory of oxygen as an environmental pressure, what is the contribution of oxygen to selection, adaptation, or survival. How much ecological variation is there between one strain of yeast and another, for example?

Why haven't you ever thought of all the things that make your presence in debate with me irrelevant? Your comments do nothing to change the fact that adaptive evolution is nutrient-dependent and pheromone-controlled. Yeast selection at the advent of sexual reproduction is for glucose uptake, you idiot.

Two days ago, this idiot wrote: "Pheromone-directed post-transcriptional evolution is his pet theory because he's on the payroll of human pheromone companies. His papers are just as convoluted and meaningless as his posts here."

I'm not denying the involvement of epigenetics and nutrient/pheromone post-transcriptional modification. I'm just wondering how you can throw these results out without a reasonable explanation.

I can throw out results that appear to attest to mutations as the cause of adaptive evolution because no evidence suggests that is possible. Adaptive evolution occurs via ecological, social, neurogenic, and socio-cognitive niche construction. There is no room for randomness or mutations at any of the levels of niche construction that are required.

What's required is reciprocity that links gene expression to behavior and back (i.e., to gene expression), as in the wolf to dog and honeybee model of nutrient-dependent pheromone-controlled adaptive evolution.

@JVK - I had no problem understanding the paper whose link you sent. While unusual in style, it made decent points on the conservation of the overall nutrient-driven epigenetic control from our unicellular ancestors to today.

But as for:

I can throw out results that appear to attest to mutations as the cause of adaptive evolution because no evidence suggests that is possible.

So you admit that you throw out any results that disagree with you - if you are an expert in the field you will know of literally thousands of papers supporting mutations as part of evolution that you must be throwing out!

Mutations plus interbreeding plus selection are used in genetic algorithms in computers with great success, so even outside of biology there is clear evidence that it IS possible. And in biology you have to throw out thousands of papers to ignore it.

And on top of that you STILL haven't explained where the present diversity of genes comes from without mutations in your model.

Did you seriously just ask "what is the contribution of oxygen to survival"?

You just went full retard.

Did you seriously just ask "what is the contribution of oxygen to survival"?

Of course not! In the context of your ridiculous theory of oxygen as an environmental pressure, I asked what is the contribution of oxygen to selection, adaptation, or survival? The context is clearly species-specific nutrient-dependent pheromone-controlled survival, not oxygen-dependent survival.

You just went full retard.

No, you just clarified that I am attempting to communicate with one. You are not going to discuss science because you believe in a ridiculous theory of mutations as the cause of adaptive evolution. No amount of science can combat that level of confused thought. For you to come back at me with a comment about oxygen simply shows how far you are willing to go to make it appear that I have erred in my representation of a model that conflicts with your opinions about adaptive evolution.

JVK: I can throw out results that appear to attest to mutations as the cause of adaptive evolution because no evidence suggests that is possible.

So you admit that you throw out any results that disagree with you...

That's not what I said, is it? I throw out results that are not supported by evidence.

- if you are an expert in the field you will know of literally thousands of papers supporting mutations as part of evolution that you must be throwing out!

"...mutations as part of evolution..."? Which part? Tell me how mutations cause adaptive evolution and I will reconsider the usefulness to science of the ridiculous theory that mutations cause anything involved in natural or sexual selection.

Play word games instead and the discussion ends. What kind of idiot rephrases what I just said to make it seem foolish? (That was a rhetorical question.)

Aerobic respiration is much more efficient than fermentation. Traits that confer the ability to take advantage of that would be selected for as the organisms that do not have that trait die off or reduce in number.

Once again, nobody ever claimed that mutations are the selective pressure. They manifest themselves in traits which can be selected for by environmental pressures, e.g., a yeast capable of floating and accessing a large oxygen supply.

Someone's been feeding the trolls again.

@JVK - Mutations providing variety for natural selection is so well documented that if you ignore that you are clearly ignoring anything the disagrees with you.

And you have YET AGAIN failed to answer where the variety of genes comes from in your mutation-free model.

@barakn - trolls must be answered or their willful ignorance will be spread throughout the land. While one cannot eliminate such trolls, one can deal with those that cross one's path.

@barakn - trolls must be answered or their willful ignorance will be spread throughout the land. While one cannot eliminate such trolls, one can deal with those that cross one's path.

Previously RealScience wrote: "@JVK - I had no problem understanding the paper whose link you sent. While unusual in style, it made decent points on the conservation of the overall nutrient-driven epigenetic control from our unicellular ancestors to today."

Now, I'm a troll, albeit with a series of published works that detail precisely how genetically predisposed nutrient-dependent species diversity is pheromone-controlled. At the same time, this idiot asks what causes the existing variety of genes in extant species, and the other idiot proposes that the cause is oxygen.

I hope someone will tell us HOW mutations are involved in anything adaptive in the context of ecological, social, neurogenic, and socio-cognitive niche construction that is required and controlled by sensory input.

@JVK - You are pretending that no one has told you how mutations are involved in evolution, yet anyone reading this thread can see that this has been answered several times. This shows clearly that you really do ignore anything that disagrees with your theory.

I asked what causes the existing variety of genes in extant species IN YOUR MODEL.

And you have YET AGAIN failed to answer where the variety of genes comes from IN YOUR MODEL.

@JVK I hope someone will tell us HOW mutations are involved in anything adaptive in the context of ecological, social, neurogenic, and socio-cognitive niche construction that is required and controlled by sensory input.

By finding a local minimum in conflict state space. Much as steel grows stronger via stimulated annealing. This works on computer models, so questioning it's efficacy is only the purview of CRANKS and religionist nutters

I asked what causes the existing variety of genes in extant species IN YOUR MODEL.

And you have YET AGAIN failed to answer where the variety of genes comes from IN YOUR MODEL.

In my model, as previously indicated, the microRNA / messenger RNA balance is responsible for the epigenetic landscape becoming the physical landscape via chromatin remodeling and de novo gene expression. Nutrient-driven changes in the balance are controlled by the metabolism of the nutrients to pheromones that control reproduction.

In the theory that idiots here think explains adaptive evolution via mutations, how is the effect of the mutations controlled? Indications are that people believe selection is for mutations.

If that's what you believe, tell me how epistasis is achieved. In my model, for example, epistasis is achieved via the epigenetic effects of nutrients on epigenetically-controlled reproduction, which is a "balanced" approach exemplified in all species.

Chromatin remodeling, as I learned it, is a method of transcription level modification- histone packing, supercoiling, etc. to induce or repress transcription.

How is that relevant to the actual base sequence of the gene?

Nutrient driven epigenetic changes are well documented, including even passing on such epigenetic changes.

Because cells are very complex, most mutations are not helpful and cells that have interactions that ameliorate the effects of many mutations survive better and are selected for. I happen to agree on the importance of RNA - I've been saying for decades RNA interaction networks control the cell, and the DNA-centric paradigm is like looking at the disk drive of a computer and ignoring the CPU.

Regarding

Indications are that people believe selection is for mutations.

I have never met anyone who believes that most mutations are selected FOR. Most mutations are either neutral or are selected AGAINST. It is a rare mutation that is useful and is thus selected FOR. And yet the accumulation of these mutation has provided the raw genetic material that the RNA networks so effectively manage.

Now where does the variety of genes comes from in YOUR MODEL?

I happen to agree on the importance of RNA - I've been saying for decades RNA interaction networks control the cell, and the DNA-centric paradigm is like looking at the disk drive of a computer and ignoring the CPU.
------------------
Now where does the variety of genes comes from in YOUR MODEL?

How many more times do I need to attribute the variety to the epigenetic effects of nutrient chemicals and their metabolism to pheromones before you grasp the factual basis of my model and compare it to whatever riduculous theory you believe in?

Chromatin remodeling, as I learned it, is a method of transcription level modification- histone packing, supercoiling, etc. to induce or repress transcription.

How is that relevant to the actual base sequence of the gene?

If you were not an anonymous idiot and I thought you might be intelligent enough to grasp the complexity of the answer to your question above, I might attempt to answer it. As it stands, however, you have not acknowledged the accurate representation of anything I've claimed in published works to date. I'm not about to recreate the model here so you can attack it from other angles without first attempting to understand it. Your question above indicates you have no idea what you're talking about, and that you cannot grasp anything new about the molecular mechanisms common to species from microbes to man.

I am not asking about the variety of the EXPRESSION of the genes, which is indeed within the realm of epigenetics.

I am asking about where the variety of the genes themselves comes from in your theory

Bloomberg News (1/25, Armstrong) reports, "The discovery, the first to identify gene mutations in the vast region of DNA that only last year was shown to have a role turning genes on and off, was published today in two studies in the online journal Science Express."
http://www.bloomb...ers.html

Here we have an example of sunlight-induced mutations that cause malignant melanoma, and the mutations are relevant to the cause of other cancers. How are the mutations selected for, or otherwise involved in adaptive evolution?

JVK: ...in the context of ecological, social, neurogenic, and socio-cognitive niche construction that is required and controlled by sensory input, this idiot states:

By finding a local minimum in conflict state space. Much as steel grows stronger via stimulated annealing. This works on computer models...

The added value here is that we have another example of an anonymous fool who thinks a contribution from another brand of nonsense is relevant to ecological, social, neurogenic, and socio-cognitive niche construction.

My name is Andrew Jones. I'm a senior at Carthage College studying biology. Non-anonymous enough for you?

Stop deflecting with back-handed insults and answer the question.

I know about epigenetics. I know about quorum sensing, which was covered extensively in microbio, which I just took in the fall. I know about DNA topology; I did a paper and presentation on it in genetics. Chromatin remodeling does not change the base sequence. How do you explain observed base sequence changes, observed point mutations, etc.?

I just picked through your paper with a fine tooth comb. I found nothing that directly contradicts the Fidalgo et al paper I linked. There was nothing that said the phenotypic effects of mutations can't result in natural selection through improved nutrient access, which the Fidalgo paper demonstrated.

Here we have an example of sunlight-induced mutations...

There are negative, neutral, and positive mutations. Fidalgo et al is a clear example of a positive one.

Here we have an example of sunlight-induced mutations that cause malignant melanoma, and the mutations are relevant to the cause of other cancers. How are the mutations selected for, or otherwise involved in adaptive evolution?

To repeat, harmful mutations are selected AGAINST.

While helpful mutations are rare, they are selected FOR.
For example, lactase persistence has been traced to mutations that have been selected FOR in societies where milk is consumed.

So once again, where does the variety of the genes themselves come from in your theory?

Does this nine year old research paper support your work?

Yes. Substantial progress has been made in determining how nutrient dependent stressors and social stressors epigenetically alter intracellular signaling and stochastic gene expression. The required receptor-mediated "molecular handshakes" and chromatin remodeling have been virtually ignored in the context of unmodelled epistatic interactions.

Since there is no model for mutations that cause adaptive evolution, it surprises me when people criticize my model of nutrient-dependent pheromone-controlled reproduction and adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction. The problem may require a paradigm shift and redefinition of what others refer to as mutations.

Is an epigenetically effected change in gene expression that is epistatically controlled by food and pheromones a mutation? Or is the unmodelled mutations theory of adaptive evolution as ridiculous as it seems?

While helpful mutations are rare, they are selected FOR.
For example, lactase persistence has been traced to mutations that have been selected FOR in societies where milk is consumed.

Lactose persistence is nutrient chemical dependent; it is not caused by a mutation in any species, and neither is genetically predisposed glucose or adaptively evolved citrate uptake the result of a mutation. Increased glucose/nutrient uptake is selected for via the metabolism of nutrients to species specific pheromones.

So once again, where does the variety of the genes themselves come from in your theory?

Stop asking that ridiculous question and look up de novo gene expression as I have repeatedly asked you and others to do. Then tell everyone that "Olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans." -- as detailed in my model.
http://dx.doi.org...i0.17338

My name is Andrew Jones. I'm a senior at Carthage College studying biology...

I know about epigenetics... I just picked through your paper with a fine tooth comb. There was nothing that said the phenotypic effects of mutations can't result in natural selection through improved nutrient access, which the Fidalgo paper demonstrated.

Increased nutrient uptake (not just access) is selected via the metabolism of nutrient chemicals to pheromones. Did the Fidalgo paper demonstrate nutrient-dependent pheromone-controlled ecological, social, neurogenic, and socio-cognitive niche construction as is required for adaptive evolution in species from microbes to man. If not, how could you have missed the fact that they did not demonstrate cause and effect, which requires the receptor-mediated "molecular handshake" et al?

If you are paying for your education, ask for a discount. Good luck, Andrew. You'll need it even if you read everything I've published. Comprehension is required.

You're going to have to be more specific when talking about the Fidalgo paper, JVK.

If you apply your model to the yeast, is oxygen the nutrient chemical? What pheromone is it metabolized to? By what enzyme(s)?

Are you also denying the selective powers of environmental pressures? Predation of incorrectly colored peppered moths inducing a founder effect seems to disagree.

So once again, where does the variety of the genes themselves come from in your theory?

Stop asking that ridiculous question and look up de novo gene expression as I have repeatedly asked you and others to do.

As I already pointed out,

I am not asking about the variety of the EXPRESSION of the genes, which is indeed within the realm of epigenetics.

I am asking about where the variety of the genes themselves comes from in your theory

I will point it out AGAIN - de novo EXPRESSION deals with variation in when genes are EXPRESSED, not with creating new genes. So if that is your only answer, then your model is incomplete.

OK. I will rush in where angels fear to tread.
Evolution will make use of the darnedest things.
There was one example of an electronic chip that designed using evolutionary programming. The result was a chip with two separate circuits on it, one of which did absolutely nothing, but when it was removed the chip did not work. Go figure.

With this in mind, why would evolution pass over the most powerful information processing ever? Quantum computing.

Consider the jumping spider. She has an amazing suite of behaviors, all of which must have been in the single cell zygote.
Or were they? That seems implausible.
Evolution probably made use of information stored in quantum states.
Why wouldn't it?
http://www.dontve...why.html

"Seek and do not stop looking until you find. When you find you will be perplexed. When Perplexed, astounded and rule over all."Christ. the Gospel of Thomas.

Since there is no model for mutations that cause adaptive evolution

.

It is hard to believe that anyone in the field would be unaware of the extensive work modelling mutations in evolution. Oh, that's right - you ignore anything that disagrees with your theory.

As for:

Lactose persistence is nutrient chemical dependent; it is not caused by a mutation in any species

, multiple mutations for persistence are known (e.g., http://www.newsde...id=1376)

So why don't you try to convince the authors of papers on Lactose-tolerance mutations instead of wasting your time here?

Oh, that's right, you claim that

People in academia already are convinced

You're going to have to be more specific when talking about the Fidalgo paper, JVK.

I will be more specific if we discuss my model as presented in my published work. I don't care what theorists have to say, and I'm not going to look back at the Fidalgo paper, since my interest is in discussion of biological facts.

The participants here have made this topic so convoluted as to defy any attempt to make sense of nutrient-dependent pheromone-controlled adaptive evolution, which is exemplified in all species. I'm happy to let you all continue in your ignorance, because I'm sure most have "weak mentalizing abilities" anyway. See for example: http://linkinghub...12002677

RealScience can't comprehend de novo expression in the context of Creation, epigenesis, or epistasis, for example. Given the ridiculous mind-set of mutations theory, there's little hope for scientific progress here.

The evidence for stress induction is found in nutrient stress and social stress. Both epigenetically effect intracellular signaling and stochastic gene expression in species from microbes to man.

Don't the authors suggest a (independent)frame shift mutation model to explain:
[That] there is no model for mutations that cause adaptive evolution? - JVK
Their suggestion put forward in their abstract and expounded on in the body of their paper?
http://connection...chanisms

Creation

Creation with a capital C, as in Creationism? You're with kevinrtrs who thinks that information can not be added to the genome. That's all I needed to know.

You just proved beyond a shadow of a doubt that I'm dealing with somebody who values dogma over evidence and now I find it extremely ironic that you tell others the same thing.

I know you'll mince my words and misinterpret this as a white flag, but I'm done.

RealScience can't comprehend de novo expression in the context of Creation, epigenesis, or epistasis, for example.

@JVK - apparantly you don't understand that the word "expression" in "de novo expression" deals with EXPRESSION of genes, not alteration of the genes themselves.

Given the ridiculous mind-set of mutations theory, there's little hope for scientific progress here.

If all you do is assume that anyone who disagrees with you doesn't understand, and ignore anything that doesn't agree with your model, then there is little hope for progress for YOU, for it means that your ignorance is willful.

What you have presented of your theory is incomplete because it does not explain where the genes themselves come from.

Creation with a capital C, as in Creationism?

I established the context. The problem is that theorists cannot address epigenesis or epistasis, which is why I placed Creation in that context. Your response is typical: attack 'Creationism' as if you had no problem with an explanation of epigenesis and epistasis via mutations theory.

You just proved beyond a shadow of a doubt that I'm dealing with somebody who values dogma over evidence....

No! You were cornered by your own dogma via my epigenetic approach. Nutrient-dependent pheromone-controlled adaptive evolution is biological fact, not dogma. Now you see that you cannot get back out of the corner with a ridiculous theory.

I know you'll mince my words and misinterpret this as a white flag, but I'm done.

Of course you are! How could you be any less of an idiot than what you have already shown yourself to be? A college education is wasted on fools who cannot accept biological facts. Please consider social science.

@JVK - You were cornered, not AROC91. Apparently you didn't understand that the word "expression" in "de novo expression" deals with EXPRESSION of genes, not alteration of the genes themselves.

As for dogma, you assume that anyone who disagrees with you doesn't understand, you ignore anything that doesn't agree with your model, and you endlessly repeat your catch phrase. That is the epitome of being dogmatic.

I've never seen a theorist have a problem with either epigenesis or epistasis. But your theory has a problem - it is incomplete because it does not explain where the genes themselves come from.

... your theory is incomplete because it does not explain where the genes themselves come from.

From the article: "...the expression of amino acid biosynthesis genes that enable bacteria to adapt to amino acid limitation is affected by the hierarchy between robust and sensitive codons."

De novo BIOSYNTHESIS of the genes expressed is dependent on the supply of nutrients. "We found that mutating codons that are perturbation robust to those that are perturbation sensitive in the leucine-biosynthesis genes... decreased their protein synthesis rate during cognate amino acid limitation, but not during amino acid-rich growth...."

Conclusions (mine)
Nonsense: mutations are involved in adaptive evolution when amino acids are scarce and also in nutrient-dependent pheromone-controlled reproduction when amino acids are plentiful.

Biology: Epigenetic effects of nutrients and pheromones on epigenesis and epistasis cause adaptive evolution and eliminate nonsensical mutations theory.

I've never seen a theorist have a problem with either epigenesis or epistasis. But your theory has a problem - it is incomplete because it does not explain where the genes themselves come from.

You're not intelligent enough to see the problem that mutation theorists have, which is that mutations cannot cause epistasis. The fact that you have also been unable to understand the concept of epigenetically driven gene biosynthesis and expression (i.e., epigenesis) leads you to ignore established biological facts while trying to tell me my model does not indicate where the variety of nutrient-dependent pheromone-controlled genes come from.

The biosynthesis of genes and their expression is discussed in the article that others WERE attempting to discuss while you focused on where the variety of genes comes from in my model at a time when probably all others are acutely aware that gene biosynthesis is nutrient-dependent, you idiot (and pheromone-controlled, you other idiots).

@JVK - It is well documented that nutrient shortages increase mutation rates in bacteria, so nutrients do play a role.

But genetic changes are plentiful enough that their statistical accumulation makes a half-decent clock. In the standard model these are from mutations, including SNPs, CNVs, inversions, transposons, viruses, and wholesale duplications and deletions.
All are observed, and natural selection has also been observed to operate on all of them.

If you think that:

Biology: Epigenetic effects of nutrients and pheromones on epigenesis and epistasis cause adaptive evolution and eliminate nonsensical mutations theory.

Then explain where all the gene variants come from without mutations, and write that up and submit it to a peer-reviewed genetics publication.

Or stick with your excuse that:

People in academia already are convinced

@JVK - It is well documented that nutrient shortages increase mutation rates in bacteria, so nutrients do play a role.

Thus, only the ignorant argue against the epigenetic effects of nutrient-dependent pheromone production that controls mutation rates.

... mutations,... All are observed, and natural selection has also been observed to operate on all of them.

No evidence suggests natural selection operates on mutations to cause adaptive evolution. Epigenetic effects of nutrients and pheromones on epigenesis and epistasis cause adaptive evolution and eliminate nonsensical mutations theory.

...explain where all the gene variants come from without mutations, and write that up and submit it to a peer-reviewed genetics publication.

I published that write-up in a peer-reviewed publication of broader scope: http://dx.doi.org...0.17338. No researcher has indicated what's wrong with nutrient-dependent pheromone-controlled adaptive evolution.

only the ignorant argue against the epigenetic effects of nutrient-dependent pheromone production that controls mutation rates.

Something we agree on.

No evidence suggests natural selection operates on mutations to cause adaptive evolution.

That's something we disagree on, and if you are well read in the field you will know of thousands of papers that disagree with you.

Epigenetic effects of nutrients and pheromones on epigenesis and epistasis cause adaptive evolution

I agree if 'cause' is replaced by 'contribute to'.

and eliminate nonsensical mutations theory

.
It is not nonsensical - selection operating on mutations has been shown to be productive in genetic algorithms. Why would evolution pass up using a useful trick?
And you are ignoring thousands of publications that say that it happens in evolution, too.

The publication link doesn't work. Is it to a GENETICS journal or another neuro/behavioral journal

http://www.socioa...ew/17338

Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. DOI: 10.3402/snp.v2i0.17338.
Previously:

No evidence suggests natural selection operates on mutations to cause adaptive evolution. Epigenetic effects of nutrients and pheromones on epigenesis and epistasis cause adaptive evolution and eliminate nonsensical mutations theory.

It really doesn't matter how many papers you think support the concept of mutational cause. It's a ridiculous theory of adaptive evolution given what is currently known about epigenetic effects on the microRNA / messenger RNA balance.

For example, even antibiotic resistance must be selected for via metabolic signals of nutrient metabolism that are species specific, which is what pheromones are. They enable self / non-self recognition, which is required.

Thanks - I already read that paper.
I certainly agree that it would be ridiculous to ignore epigenetics and RNAs; I've been arguing for decades in favor of RNAs being the regulatory engines of genetic expression, and with a great deal of sophistication in their control of the genome.

However that doesn't mean that mutations play no part.
Mutations occur, and it would be wasteful for natural selection not to take advantage of them; genetic algorithms show that even when mutations are usually harmful selection can use them, and thousands of papers support that natural selection does use them.

What is clear is that you think that using mutations is ridiculous, and so it doesn't matter to you how any papers support the role of mutations.

And after dismissively telling aroc91 to study social sciences, your prized genetics reference is to an article in "Socioaffective Neuroscience & Psychology"?
ROTFLMAO!

JVK: ...in the context of ecological, social, neurogenic, and socio-cognitive niche construction that is required and controlled by sensory input, this idiot states:

By finding a local minimum in conflict state space. Much as steel grows stronger via stimulated annealing. This works on computer models...

The added value here is that we have another example of an anonymous fool who thinks a contribution from another brand of nonsense is relevant to ecological, social, neurogenic, and socio-cognitive niche construction.

This coming from a CRANK who asserts that biology isn't subject to the laws of physics and maths. The reality is more likely that you are a domain squatter who stole/grabbed pheromones.com. This so inflated your ego that now think that your work as a humdrum technician makes you an Einstein of biology

What is your alma mater?

"On the other hand, since I don't have a degree, this may mean (to you and some others) that I have nothing of value to say, with or without peer review. Perhaps, I have no peers in academia."

James V. Kohl, May 27, 2004

@kochevnik - spot on regarding the degree and the ego trip.
JVK thinks he has no peers - LMAO!

The reality is more likely that you are a domain squatter who stole/grabbed pheromones.com. This so inflated your ego that now think that your work as a humdrum technician makes you an Einstein of biology

What's more likely is that as the co-author of "The Scent of Eros: Mysteries of Odor in Human Sexuality" (1995), I recognized the likelihood that the concept of human pheromones would someday come to the attention of others, including foolish physicists and mathematicians who will never grasp the systems complexity of biology and therefore be doomed to their ridiculous theories about cause and effect in a universe that exists because... if it didn't... it wouldn't.

...I've been arguing for decades in favor of RNAs being the regulatory engines of genetic expression, and with a great deal of sophistication in their control of the genome.

Have you published your argument for this? If not, how can anyone know whether you are simply a parrot capable of recognizing the importance of work by others and claiming it is what you've been saying all along, while at the same time you ignorantly profess mutations theory as an explanation for adaptive evolution, which is totally inconsistent from any perspective that includes biological facts. Polly want a cracker? (you bird-brained idiot.)

This research should indicate maybe we want to put the brakes on for a while before we start doing stuff like this. Andromeda strain, anyone?

Arguably, the "Andromeda strain" can evolve with or without our help. Since this stuff has been going on, it has yielded results that are incompletely understood in the context of systems biology. That's not a problem for most people, however, as they don't understand anything about anything anyway. Consequences are something that others should be forced to deal with -- as more is learned about the "hidden" genetic code.

@JVK - If I were arrogant enough to publish educated guesses I'd look like a genius for some of them and an idiot for others. In this field I simply made several bets with biologist friends.

But rather than mentioning areas where I agree with you, let's stick to the disagreement. Regarding your comment:

you ignorantly profess mutations theory as an explanation for adaptive evolution

Here I agree with >99% of geneticists that mutations are a CONTRIBUTOR to evolution. In contrast you although you admit that mutations exist, you insist that natural selection doesn't use them in spite of thousands of observations in peer-reviewed papers.

Oh, that's right - you ignore the evidence because you find it ridiculous and you ignore the real geneticists because you have no peers.
And you are dismissive to the social sciences yet your prized reference you us in arguments on genetics is to an article in "Socioaffective Neuroscience & Psychology"?

ROTFLMAO!

@JVK - If I were arrogant enough to publish educated guesses I'd look like ...an idiot....

Instead, you are parroting my position on the nutrient-dependent pheromone-controlled microRNA / messenger RNA balance.

JVK:

you ignorantly profess mutations theory as an explanation for adaptive evolution

The Parrot:

Here I agree with >99% of geneticists that mutations are a CONTRIBUTOR to evolution.

You can continue to parrot the geneticists, too, and "qualify" your comments, but it will remain obvious to others you are not providing evidence of how CONTRIBUTORS cause adaptive evolution.

Your criticisms on my publication in SNP also continue to represent only your ignorance. There was a section on molecular epigenetics in our 1996 Hormones and Behavior review, and a paper I co-authored for Neuroendocrinology Letters (2001) won an award Jaak Panksepp's group won for molecular neuroscience meets the mind. SNP publication was the next logical interdisciplinary step.

@kochevnik - spot on regarding the degree and the ego trip.
JVK thinks he has no peers - LMAO!

Do co-authors count? Do those who have cited my published works count? Human pheromones: integrating neuroendocrinology and ethology -- cited by 59; From fertilization to adult sexual behavior -- cited by 29. The scent of eros: Mysteries of odor in human sexuality -- cited by 40.

Do you know how to execute a scholar.google.com search on a name "James V. Kohl" or topic "Human pheromones"? Do you realize that our 1996 mammalian model was used as the basis for modeling hormone-organized and activated invertebrate behavior? See for example: http://www.ncbi.n...10980296

Advanced status in a Ph.D program was offered in 1992. If only I agreed that human pheromones did not exist, I would have academic credentials. Instead, I have Pheromones.com and a publication history.

I think the problem is that you do not recognize what an idiot you are to be laughing your ass off

@kochevnik - spot on regarding the degree and the ego trip.
JVK thinks he has no peers - LMAO!

@JVK I think the problem is that you do not recognize what an idiot you are to be laughing your ass off

You would be more fearsome it you learned some remedial maths. Having some credentials wouldn't hurt either, cowboy

You would be more fearsome it you learned some remedial maths. Having some credentials wouldn't hurt either, cowboy

Your ridiculous comments might be pertinent if you were able to cite any mathematical model of cause and effect that has considered epistasis as a requirement of mutation-dependent adaptive evolution. Cite something like this, for example: http://rsbl.royal...bstract. It says that: To build sensible evolutionary models, we need to know how mutations interact with each other (epistasis) and with the environment (genotype × environment interactions) to determine fitness—and even how epistatic and environmental effects interact.

Or, for contrast, cite something that you think is pertinent to the biological basis of adaptive evolution via what's already known by biologists about epigenesis and epistasis who see no need to consider adding any maths BS, or BS math from a Ph.D -- if you are one.

Probably without realizing how far this harmless looking observation goes you have touched the foundations of all science and a portion of mathematics.

Meanwhile, the news release stated: "While the system helps cells to make certain proteins efficiently under stressful conditions, it also acts as a biological failsafe, allowing the near-complete shutdown in the production of other proteins as a way to preserve limited resources."

The fact that no math was involved must annoy those who are so unfamiliar with the basic principles of biology and levels of biological organization that they can only make comments based on a ridiculous theory of mutations that somehow cause adaptive evolution. Thankfully, a mathematical model is not required to show that adaptive evolution is nutrient-dependent and pheromone-controlled. If a mathematical model were required, biologists might have learned as little as the math experts about the reality they think they are observing.

@JVK - If I were parroting you I wouldn't keep pointing out how you still haven't offered any evidence against mutations contributing to evolution.
You admit that mutations occur, and if our first-generation computer algorithms can utilize often-detrimental changes to evolve efficient solutions, we should expect nature's highly evolved genetic systems to as well. Yet in spite of that, you find the concept 'ridiculous'. Who are you to tell nature that it can't use mutations constructively?

And in spite of thousands of papers on mutations contributing to
evolution through selection, you claim that "there has never been any scientific evidence for mutation-driven selection/speciation."
Care to publish that in a genetics journal?

(And by the way, I didn't criticize your publication. What I criticized was your dismissively telling aroc91 to go into social sciences, and then your prized genetics paper being in a social-science publication. Do you REALLY not see the irony in that?)

@JVK - If I were parroting you I wouldn't keep pointing out how you still haven't offered any evidence against mutations contributing to evolution.

I've insisted there is no evidence that supports mutations as a cause of adaptive evolution. You parroted me on the microRNA/mRNA balance. You now ask that I provide evidence against a ridiculous theory that is not evidence based. What kind of idiot asks a scientist to provide evidence against a theory? That was a rhetorical question, u idiot.

But see: http://rstb.royal...abstract "...all CYP genes today arose from a single ancestor, which originated probably more than 3 billion years ago"

'increased responsiveness' to the 'environment' (diet, chemical inducers, drugs, pheromones) is the suggested cause of CYP gene conservation across 3 billion years of epigenetic cause and effect. THE SUGGESTED CAUSE IS NOT MUTATIONS!

Why don't you provide evidence that suggests mutations as cause?

Exerting a stress on a door will eventually deform or break the door. Here stress is well defined.

Cells are not doors. Nutrient and social stressors are well-detailed.

In epigenetics all the doors (molecular structures) you inherit don't always have the keys to open or shut the doors to keep out or let in external event(s).

Doors do not inherit molecular structures; cells do.

You are looking for key makers. Chromatin was to be at least one maker of keys. The search for key makers continues.

The key makers are the epigenetic effects of nutrients and the epigenetic effects of species-specific metabolites of nutrients.
Nutrient stress and social stress require new receptor-mediated protein synthesis that enables adaptation to a constantly changing sensory environment. Mutations cannot possibly cause anything that could be considered adaptive in that context, which explains why no scientific evidence suggests that they do, and why that theory is so ridiculous.

What kind of idiot asks a scientist to provide evidence against a theory?

As pointed out several times, even our simple genetic algorithms can use mutations for adaptive evolution. Mutations exist in genomes, so UNLESS you have evidence that natural selection doesn't use mutations, how can you be SO SURE that natural selection doesn't use mutations that you call the idea 'ridiculous'?

You also said that you'd be happy to explain why mutations (plus, as pointed out before that, natural selection) CAN'T cause adaptive evolution, and such an explanation (if valid) would constitute evidence that mutations and natural selection DON'T cause adaptive evolution.

So is your CERTAINTY that nature doesn't use mutations as a component in adaptive evolution based on EVIDENCE or not?

So is your CERTAINTY that nature doesn't use mutations as a component in adaptive evolution based on EVIDENCE or not?

I wrote: But see: http://rstb.royal...abstract "...all CYP genes today arose from a single ancestor, which originated probably more than 3 billion years ago"

That's evidence based. Two simultaneous mutations would be required for conservation (epistasis) or for stress-induced adaptation.
1) from the bottom up (as with nutrients)
2) from the top down (as with pheromones)

No evidence I've seen suggests that simultaneous mutations ever occur. All evidence suggests that adaptations are nutrient-dependent and pheromone-controlled. Thus, any idiot (save perhaps one like you) can see that adaptive evolution in my model is based on EVIDENCE, and there is no evidence for your ridiculous theory of mutations as cause, which is why you aren't providing any. Wait, let me recalculate that.... No, I was correct in the first place, you're an idiot! I'm CERTAIN of that!

@jvk -
So your evidence against mutations being involved in evolution is that you think that it would require SIMULTANEOUS mutations?

There are many cases of non-fatal mutations, so EVEN IF two or more mutations were involved that were only beneficial together they would NOT have to be simultaneous (or even in proximate generations). For example, the paper you linked is replete with examples of genes where even detrimental mutations that affect a protein's function have low enough harm that they could (and do) persist for generations.

... examples of genes where even detrimental mutations that affect a protein's function have low enough harm that they could (and do) persist for generations.

How do they cause adaptive evolution? Low enough harm and persistence does not indicate cause and effect to me. Is there a model for that?

Please stop to think for a minute, and determine whether you have anything intelligent to say on this topic. Few people are unfamiliar with the ridiculous mutations theory, yet only you continue to attest to how ridiculous it is.

@JVK - your evidence against evolution using mutations was that it would require simultaneous mutations.

... examples of genes where even detrimental mutations that affect a protein's function have low enough harm that they could (and do) persist for generations.

is a refutation of that.

Quoting it out of context does not change that it refutes your assumption that simultaneous mutations would be required.

Mutations exist and natural selection can apply to any variation. Even our first generation of genetic algorithms can use mutations constructively, and genomes have had time to evolve for more sophisticated control systems.

Do you have any other 'evidence' that genomes don't use mutations, or any reason to think that genomes would be so wasteful as to not use mutations?

Adaptive evolution is nutrient-dependent and pheromone-controlled.

@JVK - your evidence against evolution using mutations was that it would require simultaneous mutations.

Yes! Simultaneous mutations would be required for receptor-mediated nutrient uptake and for mutation-driven metabolism of the nutrient(s) to species-specific mutated pheromones that epigenetically effect the mutant behavior of conspecifics.

Do you have any other 'evidence' that genomes don't use mutations, or any reason to think that genomes would be so wasteful as to not use mutations?

Since there is no evidence that supports that ridiculous theory, nothing besides biological fact is required to refute it, unless you're an idiot. Whether or not you are an idiot can be evaluated based on your ability or inability to provide evidence that mutations cause adaptive evolution in the context of this discussion -- while ignoring evidence that mutations are not the cause of adaptive evolution.

Mutations "theory" is nothing more than an idiot's view of the basic principles of biology. Look up 'de novo' gene expression.

What he is trying to say is that you are not looking at the big picture. Complexity is the fundamental driving force of evolution through fractal recursive iteration. While it is true that man of this day may resort to purely adaptive evolution. There is clearly evidence to suggest that intelligence especially that resulting from integration of technology and biology will result in an intelligent purpose driven evolution.

Mutations "theory" is nothing more than an idiot's view of the basic principles of biology. Look up 'de novo' gene expression.

What he is trying to say is that you are not looking at the big picture. Complexity is the fundamental driving force of evolution through fractal recursive iteration.

No, what I'm saying is the portrayal of mutations here: http://www.forbes...unk-dna/ is a misrepresentation of cause and effect.

"Many mutations are neutral, or can be easily overcome by technology. And some of them cause a great deal of psychological suffering, such as the mutation that causes trimethylaminuria, which is physically harmless but causes the victims to smell like rotten fish no matter how clean they are."

Trimethylaminuria is genetically predisposed, nutrient-dependent and pheromone-controlled. It is common to mice, repels rats, and repels humans, which exemplifies the adaptation, not a mutation

I can see that being true. My question is, is intelligent purpose driven evolution the next paradigm shift of evolution. No one seems to be comfortable giving a clear answer to this question.

Yes! Simultaneous mutations would be required for receptor-mediated nutrient uptake and for mutation-driven metabolism of the nutrient(s) to species-specific mutated pheromones that epigenetically effect the mutant behavior of conspecifics.

@jvk - most new species are not created in one genetic change, but by the accumulation of numerous minor changes (both genetic and epigenetic). Therefore unless there is NO path of non-fatal changes that can morph the receptor or pheromone of an ancestral species to that of a descendant species, simultaneous mutations are not required. And critical genes in rapidly evolving areas often have backups that allow one copy to accumulate mutations without serious consequences to the organism.

So you still haven't provided evidence again evolution using mutations, yet you call the theory ridiculous.

So you still haven't provided evidence again evolution using mutations, yet you call the theory ridiculous.

There is no evidence that mutations cause ADAPTIVE evolution, which is why that theory is ridiculous and why you exemplify ignorance and nonsense in attempts to get me to provide you with evidence AGAINST mutation-caused adaptive evolution, when you cannot provide one example or a model in which a mutation-caused adaptation would be selected from a background of nutrient-dependent pheromone-controlled ADAPTIVE evolution which is exemplified in species from microbes to man, as detailed in my model. If you really think that mutations cause beneficial adaptations, tell us how a nutrient-induced mutation might result in something that a conspecific would select as a signal of reproductive fitness that would benefit species survival, or quit playing the fool. Despite your exemplary role-playing you are now merely annoying, you idiot.

I can see that being true. My question is, is intelligent purpose driven evolution the next paradigm shift of evolution. No one seems to be comfortable giving a clear answer to this question.

Anyone who states that clearly will be attacked for being a Creationist (as seen here earlier, when aroc91 dropped out). Such beliefs have nothing to do with proof of cause and effect from the perspective of molecular biology (the topic here), unless you are an atheist or agnostic who is relatively underinformed about the basic principles of biology and levels of biological organization required to link genes to behavior and back via sensory input. The fact that theorists must rely entirely on their theory of mutation-caused evolution when no evidence suggests mutations are adaptive is what's avoided here by the undereducated and foolish advocates of a ridiculous theory. In what has become a 5-page discussion, no evidence suggests mutations cause adaptive evolution, but fools suggest it.

@Stevepidge: Humans are already purposefully driving evolution in some species. This started with food crops and animal over 10K years ago (and perhaps considerably longer ago). Now we have started doing it even more directly, although still fairly crudely, with genetic engineering.

The numberless molecular structures of nutrients are the key makers.
The cell provides the 'workbench or bank' for key makers. Cells must have (inherit) workbenches to assist all key makers.

Why not just learn about the microRNA/messenger RNA balance and accept the obvious fact that my model is the only model for adaptive evolution -- and and quit trying to drag the discussion to one of meaningless physics and math?

The 'door' for a cell is a metaphor for any molecular structure of the cell's membrane that allows a mutual exchange of any activity between all that which is labeled external to the cell and all that which is labeled internal to the cell.

The apple is an allegorical representation of what is required for nutrient-dependent social control of adaptive evolution by the metabolism of the nutrients to species specific pheromones. The allegorical representation seems almost Biblical, doesn't it? The metaphorical/physics approach seems, at best, agnostic, which is why I think it is most often used by those who do not understand or embrace the complexity of the cell. They seem to instead want to focus on the complexity of the universe, in hopes that the unfathomable complexity of that combination with complexity of the cell will somehow reduce the focus on systems biology in adaptive evolution. Did the cosmos evolve via mutations in keys and doors?

if the bacteria are in an environment where they can grow and thrive, each synonymous codon produces the same amount of protein,..But the moment we put them in an environment where they are starved of an amino acid, some codons produce a hundredfold more proteins than others

We have a proverb: A friend in need is a friend indeed, which roughly means, the harsh conditions will reveal a true character of people. It corresponds the decreasing stability of physical and/or socioeconomic systems, which are nearing to phase transform: a noisy fluctuations will emerge, because the influence of individual factors becomes pronounced.

it also acts as a biological failsafe, allowing the near-complete shutdown in the production of OTHER PROTEINS as a way to preserve limited resources

While I do consider this study rather insightful, I feel out of logics here - are we still talking about competitive production of the SYNONYMOUS PROTEINS here? Or did I rather miss something instead?

No model is the only model for anything imagined or thought.

I wrote: "...the microRNA/messenger RNA balance ... is the only model for adaptive evolution..."

If you disagree with that statement of fact, which is made in the context of what is currently known, you need only offer another model of adaptive evolution for comparison. The theoretical approach gets us nowhere, as everyone has already seen who has followed this discussion. Sooner or later the biological facts must be addressed in the context of a ridiculous theory. Why not try that now?

You are rightfully subjected to demands of proof. Demands beyond the scope of models.

With no model, you are not subjected to demands of proof that supports a ridiculous theory, which has never been scientifically supported. This, at a time when several studies have shown that human pheromone production alters hormones and brain activity, and my own unpublished works show a behavioral affect of an androstenol/androsterone mixture in ovulatory phase women, which is precisely what one could expect if the mixture altered behavior in accord with my well-detailed model.

Now, back to you for an approach to adaptive evolution using physics and/or math, which has led to nothing neuroscientifically known about ecological, social, neurogenic, and socio-cognitive niche construction -- as is required for adaptive evolution. You have no model for that. Can you tell how adaptive evolution occurs, in theory? What is it that mutations cause that is adaptive? Where's YOUR proof?

It seems you enjoy playing devil's advocate, not because you achieve meaningful dialogue but rather because you enjoy being contrarian.

I enjoy being neuroscientifically correct in a world of theoretical nonsense. For example, see: http://www.scienc...12002141 "Even within the neurons, increasing numbers of miRNAs are being identified to regulate various stages of neuronal development and function. Not only expression of miRNAs but also the targets of miRNAs are dynamically regulated, both spatially and temporally, contributing to the diversity
and plasticity of our brain."

While fools argue that the adaptively evolved diversity and plasticity of our brain is somehow caused by mutations, it is clear that the microRNA /messenger RNA balance, which is epigenetically effected by nutrient chemicals and pheromones, causes neurogenic niche construction as part of an evolutionary continuum that is not due to mutations. Only an idiot would...

In the beginning was physics. Adaptive evolution can not occur without it. Theoretically.

At the beginning of adaptive evolution was the cell. Factually. Was the topic here the cellular genetic code, or theoretical physics? Biological sense, or NONSENSE?

What occurred before the cell? Factually. You need the origin of the cell. What is the origin of genetic code? What is origin of molecules?

The origin of the cell is not required to discuss the molecular biology of adaptive evolution, which is clearly nutrient-dependent and pheromone-controlled as I have detailed in my model. If you have a comparable model of adaptive evolution, we could discuss it. If all you have is a ridiculous theory of mutation-caused adaptive evolution, you can only compare my model to your nonsense -- as we have seen.

You must add me to your list of people that are senseless.
I insist.

I will be happy to do so, and invite others to be added if they also insist on discussing physics in the context of "A hidden genetic code: Researchers identify key differences in seemingly synonymous parts of the structure."

Clearly, if you don't know anything about the genetic code (the topic here), you should not be attempting to discuss it. I've never entered discussion of physics because I don't know anything about it, and do not need to learn anything about physics to know that adaptive evolution is nutrient-dependent and pheromone-controlled.

Thanks for your persistence and irrelevant comments, nevertheless. It's harder to make sense of the genetic code if someone is not providing nonsense in the context of physics for comparison.

http://phys.org/n...tml#nwlt

Manfred Milinski, Ilona Croy, Thomas Hummel and Thomas Boehm, Major histocompatibility complex peptide ligands as olfactory cues in human body odour assessment, Proceedings of the Royal Society B, published online January 23, 2013
doi:10.1098/rspb.2012.2889

Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors
http://dx.doi.org...i0.17338

Adaptive evolution via mutations is the most ridiculous theory ever fed to the biologically under-informed masses.

If all you have is a ridiculous theory of mutation-caused adaptive evolution, you can only compare my model to your nonsense -- as we have seen.

@JVK - It has been pointed out throughout this thread that mutations do not CAUSE adaptive evolution, but rather natural selection uses mutations as a source of variety which CONTRIBUTES to adaptive evolution.
We have also seen that both your attempts at evidence that adaptive evolution couldn't use mutations were based on incorrect assumptions on your part, and you have provided no further evidence, and your resorting to insults is evidence that you have no valid argument.

The interaction-networks molecules involved in genetics do not violate the principles of physics, chemistry and mathematics, but follow these principles themselves as they use these principles to organize and control other molecules.

- continued-
As for evidence in favor of evolution using mutations, in addition to the thousands of paper that you surely must know of if this is your field, this thread already contains evidence.
First, even our crude computational genetic algorithms already use typically-harmful mutations, so clearly a highly -evolved system COULD also use them. And even you admit that mutations exist, so it would be wasteful for evolution NOT to use them.
Supporting this are that the equivalent of mutations have been found useful in a wide variety of complex optimization, including the routing of the computer and networking chips you use to type your comments on and send them in with.
Yet you still think that nature's highly evolved systems using them is ridiculous.

-continued-
Furthermore the overview on CYP genes that you sent shows that genomes have evolved mechanisms for allowing many mutations to remain in a genome. The stasis feedbacks you refer to cover so well for many mutations that those mutations can persist for generations, and in areas where stasis would be difficult the CYP family provides multiple redundancy that allows major mutations to accumulate even in critical genes.
Accumulation mutations are far from random because life has evolved to evolve. Key areas of the genome are more mutation resistant, and the genomes repair capabilities also more diligently repair key area. This again lowers the penalty for allowing mutations to accumulate.
That genomes go to such lengths to allow mutations to accumulate is itself evidence that genomes have some use for them.
No use has been found other than natural selection, which can use any source of variety so it benefits from those mutations.

- continued -
Since natural selection can use any source of variety, it is clear that natural selection WOULD use mutation-initiated variety to drive adaptive evolution if it were possible to do so.
That even our crude genetic algorithms can use mutations and natural selection to drive adaptive evolution is evidence that it is not impossible.
That genomes have evolved ways to use mutations to accumulate variety, and that no other use than natural selection has been found adds weight to that evidence.
Since you have failed to provide ANY evidence that genomes can't use mutations in adaptive evolution (other than calling it ridiculous), the evidence from this thread alone is heavily in favor of mutations be used by adaptive evolution.

Are there ALSO other things used in addition to mutations?
Certainly, and no one in this thread has questioned that.

Thanks for a lengthy explanation of nothing neuroscientifically known. What's known is that adaptive evolution is nutrient-dependent and pheromone-controlled. You need only tell us how mutations cause something that is selected for, but you cannot. What is the point to your continued promotion of a ridiculous theory?

- continued -
Since natural selection can use any source of variety, it is clear that natural selection WOULD use mutation-initiated variety to drive adaptive evolution if it were possible to do so.

How does natural selection use ANY source of variety? Why would selection occur for a mutation? What is it about adaptive evolution that you think makes that possible? Stop the ridiculous diatribes on algorithms and address the biological facts, since algorithms cause nothing more than confusion in the context of biological facts that link sensory input directly to genes and behavior and back.

Natural selection does not care where variety comes from, it simply amplifies whatever works better, and diminishes whatever works less well, relative to each other.
Selection occurs FOR a mutation in a circumstance where that mutation offered an advantage.
Sickle-cell mutations are an example - a handful of different variations are known that offer an advantage in regions where malaria is endemic and a disadvantage in regions where it isn't.

I have presented evidence that evolution should be able use mutations, plus evidence that genomes have evolved to ACCUMULATE variety from mutations. (And you have never denied knowing of thousands of papers that claim evidence that it does use mutations). In contrast you have provided NO evidence that it does not use mutations.
Why would genomes evolve to accumulate something potentially harmful if they couldn't use it? You greatly underestimate how 'smart' genomes have evolved to be.

Natural selection does not care where variety comes from...

If the variety has nothing to do with nutrient uptake or pheromone-controlled reproduction, natural selection cannot select. There are no molecular mechanisms that allow selection for non-olfactory/pheromonal input -- unless the response has already been conditioned to occur via olfactory/pheromonal input.

Why would genomes evolve to accumulate something potentially harmful if they couldn't use it? You greatly underestimate how 'smart' genomes have evolved to be.

You greatly underestimate your ignorance. See for example: Gene duplication as a mechanism of genomic adaptation to a changing environment http://rspb.royal...full.pdf "One of the main duplicated gene families are the olfactory receptor proteins..."

If the variety has nothing to do with nutrient uptake or pheromone-controlled reproduction, natural selection cannot select.

If the variety has ANYTHING to do with reproduction (including surviving long enough to reproduce, having offspring that in turn reproduce, or even relatives that reproduce, etc.), then natural selection can select.

There are no molecular mechanisms that allow selection for non-olfactory/pheromonal input...

I just gave you the example sickle-cell example, in which molecular changes to hemoglobin are selected for, when malaria is prevalent, in spite of INTERFERING with oxygen uptake.

The paper you cited CONTRADICTS your posts, detailing how duplication mutations of non-nutrient-uptake/pheromone genes can have positive impact (e.g., cold resistance).
Furthermore in the section on Pranting & Andersson's work the paper you cite clearly describes mutations having a role in antibiotic resistance in evolution.

I have presented evidence that evolution should be able use mutations, plus evidence that genomes have evolved to ACCUMULATE variety from mutations.

What you have done is repeatedly present the same ridiculous theory with no evidence, and no citations to any published work from anyone who knows HOW mutations cause adaptive evolution. If your intent was to make a fool of yourself, you have succeeded.

If the variety has ANYTHING to do with reproduction (including surviving long enough to reproduce, having offspring that in turn reproduce, or even relatives that reproduce, etc.), then natural selection can select.

selection can select FOR WHAT?

I just gave you the example sickle-cell example, in which molecular changes to hemoglobin are selected for...

selected for HOW?

Furthermore in the section on Pranting & Andersson's work the paper you cite clearly describes mutations having a role in antibiotic resistance in evolution.

WHAT ROLE IS THAT? HOW DOES THEIR "ROLE" ALLOW MUTATIONS TO CAUSE ADAPTIVE EVOLUTION?

You're not very bright, are you? Someone told you a story about a theory, and not only did you believe it, but you're trying to tell others that ridiculous theory without realizing how ridiculous it is.

What you have done is repeatedly present the same ridiculous theory with no evidence, and no citations to any published work from anyone who knows HOW mutations cause adaptive evolution.

Repetition:
You repeatedly stated that mutations don't cause adaptive evolution, and that the idea is ridiculous.
In response it has been repeatedly pointed out to you that mutations CONTRIBUTE to evolution rather than CAUSE it, along with evidence.

Evidence:
Reader of this thread can see that multiple lines of evidence have been provided AGAINST your assertion that evolution doesn't use mutations.
The few times that YOU have presented 'evidence' it has been shown to be based on false assumptions (e.g., requiring simultaneous mutations).

Citations:
I cited back papers that you linked, since they provided ample evidence AGAINST your assertion.

Insults:
Insults generally show a lack of arguments, and readers can decide for themselves whether your insults apply better to me or to yourself.

selection can select FOR WHAT?

Select for increased representation in that species genome.

selected for HOW?

By people with that mutation averaging more children that themselves survive to reproduce (in the sickle-cell example this is due to greater resistance to malaria).

If you really didn't already know the answers, then you don't even understand the theory you are calling ridiculous.

WHAT ROLE IS THAT? HOW DOES THEIR "ROLE" ALLOW MUTATIONS TO CAUSE ADAPTIVE EVOLUTION?

Did you even read the paper you linked?
It describes a series of mutations: first a point mutation provides resistance to an antibiotic peptide but at a cost in growth, then a gene duplication mutation then decreases the growth cost, and finally after additional point mutations provide resistance without impairing growth, the extra gene is selected against.
More details can be found in the P&A paper itself: http://onlinelibr...58.x/pdf

I am fascinated by your explanation of WHAT is selected and HOW selection occurs (it's so automagical!):

Select for increased representation in that species genome.By people with that mutation averaging more children that themselves survive to reproduce (...due to greater resistance...).

Are you saying that increased representation automagically occurs when mutations result in more offspring via a series of mutations that cause greater resistance?

first a point mutation provides resistance to an antibiotic peptide...then a gene duplication mutation then decreases the growth cost, and... additional point mutations provide resistance without impairing growth, the extra gene is selected against.

Is there a mathematical model for how all these mutations somehow result in the 4-6 million epistatically linked DNA switches of the evolved human genome?

I'm saying that selection for nutrients leads to selection of pheromones that signal fitness.

Did you earn your GED yet?

Are you saying that increased representation automagically occurs when mutations result in more offspring via a series of mutations that cause greater resistance?

Are you SERIOUSLY saying that you don't understand how more offspring would result in increased representation? Do you understand multiplication?

I'm saying that selection for nutrients leads to selection of pheromones that signal fitness.

No one in this thread has disagreed with that being PART of evolution.

Did you earn your GED yet?

Can't you at least find ONE insult that isn't about yourself?

"On the other hand, since I don't have a degree, this may mean (to you and some others) that I have nothing of value to say, with or without peer review. Perhaps, I have no peers in academia." James V. Kohl, May 27, 2004

Notice that I quoted it in full instead of taking it out of context as you would (i.e., "I have nothing of value to say", James V. Kohl).

JVK:

Are you saying that increased representation automagically occurs when mutations result in more offspring via a series of mutations that cause greater resistance?

RealScience

Are you SERIOUSLY saying that you don't understand how more offspring would result in increased representation?

JVK: Of course not. I'm asking how mutations contribute to increased representation.
RealScience

Do you understand multiplication?

JVK: Of course. That's why

I'm saying that selection for nutrients leads to selection of pheromones that signal fitness.

Multiplication is unequivocally dependent on two things: Nutrients and pheromone-controlled reproduction. If mutations were involved, you might be able to tell me how mutations enabled nutrient uptake and how nutrient metabolism epigenetically effected reproduction to contribute to adaptive evolution. Instead you continue to tell me that mutations do something... somehow. In theory, they increase representation. HOW?

JVK: Of course not. I'm asking how mutations contribute to increased representation.

Some mutations allow a creature to live longer or healthier and have more opportunities to have offspring, and thus on the average have more offspring.
I already provided the example of sickle-cell mutations reducing susceptibility to malaria and thus increasing reproductive opportunities when malaria is prevalent. The P&A paper I cited details how mutations can increase antibiotic resistance, thus increasing reproductive opportunities when antibiotics are present. Even the Kondrashov paper you cited showed that mutations can increase cold resistance, which opens up new habitats and reproductive opportunities.

As can be seen in the above examples, multiplication is dependent on surviving long enough to reproduce AS WELL AS on nutrients and detecting potential mates.

And it is SELECTION that increases representation of some mutations.

JVK: I'm asking how mutations contribute to increased representation.

RealScience:Even the Kondrashov paper you cited showed that mutations can increase cold resistance, which opens up new habitats and reproductive opportunities.

The new habitats are nutrient-dependent ecological niches, which are responsible for pheromone-controlled social niche construction.

RealScience:As can be seen in the above examples, multiplication is dependent on surviving long enough to reproduce AS WELL AS on nutrients and detecting potential mates.

REPRODUCTION is nutrient-dependent and pheromone-controlled. If you want to tout mutation-caused "multiplication" via organisms surviving long enough to reproduce, you must introduce an effect of the mutation. What does the mutation cause that alters selection?

And it is SELECTION that increases representation of some mutations.

Selection for WHAT? HOW is the genetically-predisposed epistasis of cold-resistance selected?

RealScience:Even the Kondrashov paper you cited showed that mutations can increase cold resistance, which opens up new habitats and reproductive opportunities.

The new habitats are nutrient-dependent ecological niches, which are responsible for pheromone-controlled social niche construction.

And the mutation that increases cold resistance allows the cold-tolerant fish to use that new niche, so the mutation CONTRIBUTES to the adaptive evolution.

you must introduce an effect of the mutation. What does the mutation cause that alters selection?

In the examples given, the effects that the mutations caused were increased resistance to malaria, increased resistance to antibiotics, and increased resistance to cold.

Selection for WHAT? HOW is the genetically-predisposed epistasis of cold-resistance selected?

By the fish being able to access new food sources and better escape from less-cold-tolerant predators and thus have more offspring.

Your approach is a silly circular argument. The requirement is not met for an effect of the sensory environment on genes and on behavior that effects genes (i.e., epistatic control from genes to behavior and back).

...the mutation...allows the cold-tolerant fish to use that new niche, so the mutation CONTRIBUTES to the adaptive evolution.

What caused the MUTATION that you now say CONTRIBUTES to adaptive evolution instead of CAUSES evolution? What was mutated; how did it affect behavior and species divergence (epistasis)?

I asked

What does the mutation cause...?

You now infer that

...the mutations caused... increased resistance to malaria, increased resistance to antibiotics, and increased resistance to cold.

Is there a model for that?

I asked

HOW is the genetically-predisposed epistasis of cold-resistance selected?

By the fish being able to access new food sources and better escape from less-cold-tolerant predators and thus have more offspring.

RealScience needs help with the requirement for an effect of the sensory environment (i.e., epistatic control from genes to behavior and back). Is there not one among the evolutionary theorists who can tell us HOW a mutation contributes to adaptive evolution (e.g., by allowing cold-tolerant fish to use a new niche)? Can anyone tell us anything about any MUTATION that CONTRIBUTES to adaptive evolution instead of CAUSES evolution, or how that mutation affects behavior and species divergence (epistasis)?

I've asked

What does the mutation cause...? HOW is the genetically-predisposed epistasis of cold-resistance selected? Is there a model for that?

So far, we've learned that something causes a mutation that somehow allows fish

...to access new food sources and better escape from less-cold-tolerant predators and thus have more offspring...

But that just attests to how ridiculous that theory actually is because it explains nothing via biological cause and effect.

Target article except: "...seemingly synonymous parts of the genetic code are anything but. Under some stressful conditions, the researchers found, certain sequences manufacture proteins efficiently, while others—which are ostensibly identical—produce almost none."

Nutrient stress is the variable. Adaptive evolution is nutrient-dependent and pheromone-controlled in species from microbes to man. How can it not be clear that the epigenetic effects of pheromones control the epigenetic effects of nutrients in stressful and non-stressful conditions? How can anything be clarified via belief in a ridiculous theory of evolution where mutations are responsible for something adaptive? No scientific evidence suggests that is even a remote possibility, let alone a possibility that would result in 4-6 million interactive DNA switches in the adaptively evolved human genome.

Damn it, I just had to drag myself back into this.

http://www.nature...238.html

Peppered moths. Point mutation identified. Obvious natural selection through predation.

You should know that DNA pol. has a documented error rate that leads to sequence changes. If it's in a coding region, it's going to result in an altered gene product, in this case, a higher amount of pigment, which makes it darker, which allowed it to blend in during Britain's industrial revolution when its ecological niche changed due to the increased soot, which allowed it to avoid predation.

Sexual selection isn't he only selective pressure.

Is there not one among the evolutionary theorists who can tell us HOW a mutation contributes to adaptive evolution (e.g., by allowing cold-tolerant fish to use a new niche)?

Did you read the P&A paper I cited? It documents the mechanisms in great detail.
Did you EVEN READ the Kondrashov paper YOU cited? The paragraph on the bottom left of page 3 gives the details.

But that just attests to how ridiculous that theory actually is because it explains nothing via biological cause and effect.

Again, READ the papers.

...I just had to drag myself back into this.
http://www.nature...238.html
Peppered moths. Point mutation identified. Obvious natural selection through predation.

Do we now have predators causing mutations and adaptive evolution? Where's the part that addresses epigenetic control of protein synthesis by stress?

... a documented error rate that leads to sequence changes.[and]... makes it darker, which allowed it to blend in...when its ecological niche changed due to the increased soot, which allowed it to avoid predation.

Those that avoided predation were selected for by their nutrient-dependent pheromone production, not by the change in color.

Sexual selection isn't he only selective pressure.

That's why I keep saying that selection is nutrient-dependent and pheromone-controlled, and not due to mutations. You use the insect that defined the term pheromones. Moths that aren't eaten, eat and produce pheromones, you fool.

Did you read the P&A paper I cited? It documents the mechanisms in great detail.

Clearly, you have no idea what the mechanisms are.

Did you EVEN READ the Kondrashov paper YOU cited? The paragraph on the bottom left of page 3 gives the details.

Are you trying to tell me that gene duplication is not nutrient-dependent and pheromone-controlled? "One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.' -- Kondrashov (as in conditions of nutrient stress or social stress -- Kohl, 2012, and the nutrient stress in the target article).

[your]...theory... explains nothing via biological cause and effect.

Again, READ the papers.

Why, you're comments only indicate your inability to the comprehend biological facts.

Do we now have predators causing mutations and adaptive evolution?

No, we have always had both mutations and predators CONTRIBUTING to adaptive evolution. Do you REALLY not know that predators contribute to selection?

That's why I keep saying that selection is nutrient-dependent and pheromone-controlled, and not due to mutations.

Did you missed the section of the article about "providing strong evidence that natural selection had acted recently on an advantageous mutation from one individual"?

Oh, that's right:

"I can throw out results that appear to attest to mutations as the cause of adaptive evolution" - JVK

Do we now have predators causing mutations and adaptive evolution? Where's the part that addresses epigenetic control of protein synthesis by stress?

You are GROSSLY misinterpreting this. The predators don't CAUSE the mutation. The mutation produces variety on which the predators act as a selection mechanism.

Those that avoided predation were selected for by their nutrient-dependent pheromone production, not by the change in color.

No, they were selected for by NOT BEING EATEN. If a predator selectively eats one variety BECAUSE IT CANNOT SEE THE OTHER, that has NOTHING to do with pheromone production and selective mating and everything to do with merely NOT DYING.

Moths that aren't eaten, eat and produce pheromones, you fool.

How does that have anything to do with not being eaten in the first place?

'the peppered moth's genetics will "complete the package" of research on "the best example of adaptation involving natural selection that we have" http://www.nature...238.html

And yet, as we've seen with aroc91, even the best example will do nothing to undo the damage to his intellectual capacity that has been caused by his belief in a ridiculous theory of mutation-driven evolution, which is in reality nutrient-chemical AND pheromone-dependent as exemplified most clearly in insects.

For example, I used the honeybee model organism to link microbes to man in my model. What the queen eats determines her pheromone production and everything else about the behavior of every organism in the colony -- including the neuroanatomy of the nutrient-dependent pheromone-controlled adaptive evolution of the worker bees' brains. The honeybee model developed based on our mammalian model (1996)-- cited in http://www.ncbi.n...10980296 -- you fools!

The honeybee model is fine and dandy, but it has nothing to do with predation.

Are you trying to tell me that gene duplication is not nutrient-dependent and pheromone-controlled? "One of the main duplicated gene families are the olfactory receptor proteins [18,117–119] so perhaps their duplication may lead to an increase in sensitivity to a particular odour may be adaptive under certain conditions.'

That gene duplications can impact nutrients and pheromones does not imply that nutrients and pheromones control all gene duplications (although as previously pointed out, mutation rates increases under stress).
And the article attributes gene duplications to mutations:

"As any mutation, a duplication event by itself may also have consequences on organism's fitness."

You are GROSSLY misinterpreting this. The predators don't CAUSE the mutation.

That's why I asked

Where's the part that addresses epigenetic control of protein synthesis by stress?

The mutation produces variety on which the predators act as a selection mechanism.

And then, natural selection automagically selects with no attention paid to sexual selection in the context of adaptive evolution. Right? You fool! You don't get to adaptive evolution via natural selection alone.

If a predator selectively eats one variety BECAUSE IT CANNOT SEE THE OTHER, that has NOTHING to do with pheromone production and selective mating and everything to do with merely NOT DYING.

Moths that aren't eaten, eat and produce pheromones...

Selective mating is pheromone-dependent in the moths that aren't eaten (dying or dead). Natural selection (for food) and sexual selection (for pheromones) are required for adaptive evolution that you would like to be mutation-driven.

This is about selective predation based on the fact that the predator can't see certain phenotypes, not selective mating. What's automagical about camouflage?

The honeybee model is fine and dandy, but it has nothing to do with predation.

The honeybee model organism represents the epigenetic tweaking of immense gene networks in superorganisms that solve problems through the exchange and the selective cancellation and modification of signals (pheromonal, visual, auditory). It also exemplifies the fact that olfaction and odor receptors provide a clear evolutionary trail that can be followed from unicellular organisms to insects to humans.

You are correct, however, it has nothing to do with mutations and predation-driven evolution, because mutations do not drive adaptive evolution via predation. Adaptive evolution is nutrient-dependent and pheromone-controlled.

And the article attributes gene duplications to mutations: "As any mutation, a duplication event by itself may also have consequences on organism's fitness."

Look up the word 'conflation'. "...any mutation..." is different from "...a duplication event..." above, and in reality (my reality, not yours). It's the nutrient-dependent pheromone-controlled duplications that epigenetically effect the organism's fitness as exemplified in adaptive evolution. Mutations may have consequences, of course, but they do not cause evolution. No molecular mechanisms enable that. The molecular mechanisms enable nutrient-dependent pheromone-controlled adaptive evolution in species from microbes to man.

This is about selective predation based on the fact that the predator can't see certain phenotypes, not selective mating. What's automagical about camouflage?

It's role in nutrient-dependent pheromone-controlled sexual selection. Suddenly, you have visual stimuli that are primarily involved in altering the course of nutrient-dependent pheromone-controlled evolution. Is there a model for that?

What molecular mechanisms are directly effected by the camouflage? Why doesn't their camouflage make deer hunters invisible to deer, you idiot? There's a model for that!

This is about selective predation based on the fact that the predator can't see certain phenotypes, not selective mating. What's automagical about camouflage?

It's role in nutrient-dependent pheromone-controlled sexual selection. Suddenly, you have visual stimuli that are primarily involved in altering the course of nutrient-dependent pheromone-controlled evolution. Is there a model for that?

What molecular mechanisms are directly effected by the camouflage? Why doesn't their camouflage make deer hunters invisible to deer, you idiot? There's a model for that!

So the change in color (which beautifully corresponds to the changing environment color, hmmm...) is just coincidental to a simultaneous odor change that prevents predators from tracking the moths?

I suppose animals that can change their color and patterns on the fly (chameleons and cephalopods) also change their pheromone signatures on the fly as well and that's what allows them to hide?

http://beheco.oxf...abstract

http://rsbl.royal...326.full

http://rspb.royal...full.pdf

@JVK - in genetics gene duplication events are considered a type of mutation.
And you haven't addressed sickle cell mutations, which are not duplications, or the post-duplication mutations restoring fitness in the P&A paper.

@JVK - in genetics gene duplication events are considered a type of mutation.

Great, what causes the mutation? How does it enable evolution? How is epistasis achieved as a result of the mutation?

And you haven't addressed sickle cell mutations, which are not duplications, or the post-duplication mutations restoring fitness in the P&A paper.

If the sickle cell mutation is selected for, the children that result from that selection would not be as reproductively fit, would they? Why would I address the sickle cell mutations when they exemplify only a foolish theory about mutation caused evolution -- and in only one species? What kind of idiot brings up evidence like that, or like the moth species? Predation in moths, selection for sickle cell mutations...? Is there a connection there somewhere that fits within the context of the target article here -- or in the context of the continuum of adaptive evolution?

http://beheco.oxfordjournals.org/content/16/1/25.abstract

Stop playing the fool. I'm not about to read about camouflage and the role of visual input in evolution. There are too many species with no eyes, or that use olfactory/pheromonal input to condition their responses to other sensory input. I have a series of published works that does not misrepresent the facts. No reason to keep posting links to misrepresentations.

I suppose animals that can change their color and patterns on the fly (chameleons and cephalopods) also change their pheromone signatures on the fly as well and that's what allows them to hide?

I suppose you are unable to grasp the concept of genetically predisposed nutrient-dependent pheromone-controlled adaptive evolution via ecological, social, neurogenic, and socio-cognitive niche construction, and would like to waste time discussing the relative salience of visual input across the evolutionary continuum.

At some point, however, we get back to the cave fish and eye regression when the only thing important to survival is finding food and controlled reproduction so that the fish do not out-reproduce their food supply. Chemical ecology determines nutrient acquisition and metabolism to pheromones that control reproduction in species from microbes to man. Discussion of chameleons and cephalopods is a waste of time, outside that context.

Evidence outside of the context of your model is irrelevant just because it doesn't fit your model? Jesus fucking Christ. That's the definition of dogma.

Why would I address the sickle cell mutations when they exemplify only a foolish theory about mutation caused evolution

You should address because it is presented as evidence against your claim of NO role for mutations in adaptive evolution.

You have asked how mutations could be selected for.
Sickle cell mutations are selected for in the presence of malaria because ONE copy of a sickle-cell-mutation gene provides considerable resistance against malaria while only slightly decreasing fitness from oxygen transport. While the individual children are less fit in the absence of malaria, when malaria is prevalent average fitness of a carrier is raised.
Furthermore in malaria-prevalent regions humans have evolved to have a high enough occurrence of sickle-cell genes that having one copy is common while having two copies is less common, an example of adaptive evolution using mutations.

Evidence outside of the context of your model is irrelevant just because it doesn't fit your model?

No. You've offered no evidence of mutation-caused evolution, and there's no model for that.

It's your belief in a ridiculous theory of mutations, which was not evidence-based even when it was first proposed --

That's the definition of dogma.

-- especially in the context of what is now known about the molecular mechanisms common to all species.

Adaptive evolution is nutrient-dependent and pheromone-controlled!

Educate yourself: Kohl, J.V. (2012) Human pheromones and food odors: epigenetic influences on the socioaffective nature of evolved behaviors. Socioaffective Neuroscience & Psychology, 2: 17338. http://dx.doi.org...i0.17338

Why would I address the sickle cell mutations when they exemplify only a foolish theory about mutation caused evolution

You have asked how mutations could be selected for.
Sickle cell mutations are selected for in the presence of malaria because ONE copy of a sickle-cell-mutation gene provides considerable resistance against malaria while only slightly decreasing fitness from oxygen transport. While the individual children are less fit in the absence of malaria, when malaria is prevalent average fitness of a carrier is raised.
Furthermore in malaria-prevalent regions humans have evolved to have a high enough occurrence of sickle-cell genes that having one copy is common while having two copies is less common, an example of adaptive evolution using mutations.

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

Like the moth example, a resistance to malaria is beneficial in the sense of even making it to mating age in the first place. Sexual selection is not the only selective factor. Surviving up to that point is a selective factor in itself.

Without giving me some runaround copy pasted blurb, answer the question:

So the change in color (which beautifully corresponds to the changing environment color, hmmm...) is just coincidental to a simultaneous odor change that prevents predators from tracking the moths?

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

Are you SERIOUSLY saying that you don't understand this?

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

@JVK - are you SERIOUSLY asking that?
With or without pheromones, someone who is alive and fairly healthy will generally have more offspring than someone who is dead or very unhealthy.

No one in this thread has said that nutrients and pheromones are not INVOLVED. Being alive and healthier makes one better able to find food and synthesize pheromones, but that is an EFFECT rather than a CAUSE of the genetic change.

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

@JVK - are you SERIOUSLY asking that?
With or without pheromones, someone who is alive and fairly healthy will generally have more offspring than someone who is dead or very unhealthy.

No one in this thread has said that nutrients and pheromones are not INVOLVED. Being alive and healthier makes one better able to find food and synthesize pheromones, but that is an EFFECT rather than a CAUSE of the genetic change.

Exactly.

Without giving me some runaround copy pasted blurb, answer the question:

So the change in color (which beautifully corresponds to the changing environment color, hmmm...) is just coincidental to a simultaneous odor change that prevents predators from tracking the moths?

That's a ridiculous comment; not a question. I've already said that observed changes are not evidence of mutation-caused adaptive evolution -- and probably cited Dobzhansky (1972) -- as what you refer to as "some runaround copy pasted blurb". You seem to be unfamiliar with the literature, or incapable of grasping anything but a ridiculous theory. Feel free to discuss the theory with RealScience, as he may be the only other fool here who has not yet realized the level of ignorance you have both displayed.

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

Like the moth example, a resistance to malaria is beneficial in the sense of even making it to mating age in the first place. Sexual selection is not the only selective factor. Surviving up to that point is a selective factor in itself.

Surviving up to that point is nutrient-dependent. At that point, species survival is pheromone-dependent, which is why there is no model for mutation-driven speciation. Species diversity is nutrient-dependent and pheromone-controlled, but you are not intelligent enough to grasp the obvious. Unfortunately, that's typical of many atheists. See for example: The origins of religious disbelief http://linkinghub...12002677 Your "weak mentalizing ability" extends to pointless discussion here.

With or without pheromones, someone who is alive and fairly healthy will generally have more offspring than someone who is dead or very unhealthy.

No one in this thread has said that nutrients and pheromones are not INVOLVED. Being alive and healthier makes one better able to find food and synthesize pheromones, but that is an EFFECT rather than a CAUSE of the genetic change.

Cause and effect must be modeled from genes to behavior and back to explain species diversity. In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation in hormone-secreting nerve cells of the brain and the hormones affect behavior that is rewarded via its effects on genes in hormone-secreting cells.... Visual and auditory input does not directly effect genes in hormone-secreting nerve cells of the brain, so it cannot be directly linked to hormone organization or hormone-activation of behavior. It can be linked via olfaction to classical conditioned behavior.

How would I find or select a mate with the sickle cell trait? Do they have different colored wings to help them avoid predation, like moths?

Like the moth example, a resistance to malaria is beneficial in the sense of even making it to mating age in the first place. Sexual selection is not the only selective factor. Surviving up to that point is a selective factor in itself.

Surviving up to that point is nutrient-dependent. At that point, species survival is pheromone-dependent, which is why there is no model for mutation-driven speciation. Species diversity is nutrient-dependent and pheromone-controlled

It's also NOT DYING FROM MALARIA-dependent.

In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation

You have been presented with a mutation (sickle cell) that is a gene sequence alteration, which is selected FOR in adaptive evolution, and thus CONTRADICTS your statement that mutations play NO ROLE in adaptive evolution.

(You keep trying to change the discussion to something that no one is arguing with. No one in this thread has argued against feedback and epigenetics being that being PART of the picture. )

Regarding your reply to: "resistance to malaria is beneficial in the sense of even making it to mating age in the first place ... Surviving up to that point is a selective factor in itself."

Surviving up to that point is nutrient-dependent.

DO you REALLY think that surviving to a mating age depends ONLY on nutrients?

It's also NOT DYING FROM MALARIA-dependent.

I wrote: "Cause and effect must be modeled from genes to behavior and back to explain species diversity. In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation in hormone-secreting nerve cells of the brain and the hormones affect behavior that is rewarded via its effects on genes in hormone-secreting cells...." The sickle cell trait or the disease has nothing to do with cause and effect.

JVK:

In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation

idiotScience

You have been presented with a mutation (sickle cell) that is a gene sequence alteration, which is selected FOR in adaptive evolution, and thus CONTRADICTS your statement that mutations play NO ROLE in adaptive evolution.

I wrote: "Cause and effect must be modeled from genes to behavior and back to explain species diversity. In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation in hormone-secreting nerve cells of the brain and the hormones affect behavior that is rewarded via its effects on genes in hormone-secreting cells...." The sickle cell trait or the disease has nothing to do with cause and effect.
idiotScience

DO you REALLY think that surviving to a mating age depends ONLY on nutrients?

Of course not. That's why I used the honeybee model organism of pheromone-dependent brain development.

@JVK: Since you are trying to take things out of context again, I'll be more specific:

Regarding "resistance to malaria is beneficial in the sense of even making it to mating age in the first place ... Surviving up to that point is a selective factor in itself.", you replied:

Surviving up to that point is nutrient-dependent.

Step 1:
Do you think nutrition is the ONLY factor that influences whether humans survive to a mating age in a region where malaria is prevalent?

Do you think nutrition is the ONLY factor that influences whether humans survive to a mating age in a region where malaria is prevalent?

I wrote: "Cause and effect must be modeled from genes to behavior and back to explain species diversity. In vertebrates and invertebrates for example, olfactory/pheromonal input causes gene activation in hormone-secreting nerve cells of the brain and the hormones affect behavior that is rewarded via its effects on genes in hormone-secreting cells...." The sickle cell trait or the disease has nothing to do with cause and effect.

I saw what you wrote, but it does not answer the question.

I asked a very clear question:

Do you think nutrition is the ONLY factor that influences whether humans survive to a mating age in a region where malaria is prevalent?

Try providing an equally clear answer.

I saw what you wrote, but it does not answer the question.

I asked a very clear question:

Do you think nutrition is the ONLY factor that influences whether humans survive to a mating age in a region where malaria is prevalent?

Try providing an equally clear answer.

Do you think that asking such ignorant questions accomplishes anything pertinent to discussion of genetics and adaptive evolution?

@JVK -
As evidence of sickle-cell mutations being selected for, aroc91 and I wrote:

a resistance to malaria is beneficial in the sense of even making it to mating age in the first place... Surviving up to that point is a selective factor in itself.

and

With or without pheromones, someone who is alive and fairly healthy will generally have more offspring than someone who is dead or very unhealthy.

You answered:

Surviving up to that point is nutrient-dependent.

Since your answer doesn't disagree with sickle-cell mutations being selected for UNLESS you are claiming that nutrients are the ONLY factor, it is indeed pertinent to ask a very clear question:

Do you think nutrition is the ONLY factor that influences whether humans survive to a mating age in a region where malaria is prevalent?

As evidence of sickle-cell mutations being selected for, aroc91 and I wrote:

a resistance to malaria is beneficial in the sense of even making it to mating age in the first place... Surviving up to that point is a selective factor in itself.

and

With or without pheromones, someone who is alive and fairly healthy will generally have more offspring than someone who is dead or very unhealthy.

Neither of you has sufficient knowledge for me to continue discussion. There is plenty of data to support my position on nutrient-dependent pheromone-controlled non-random adaptive evolution, but none to support mutations theory. Read something current, and learn how foolish you are. Like this: http://dx.doi.org...3.01.003 Regulation of gene expression in mammalian nervous system through alternative pre-mRNA splicing coupled with RNA quality control mechanisms.

Let me know if ever you have a clue about what's required for adaptive evolution.

Sickle-cell mutations being selected for IS data supporting that mutations have a role in evolution.

Since you fail to make a counter argument, anyone reading this thread will know that you have none to make and are conceding the point (even if you lack the honor to do so publicly).

And conceding the point means that YOUR CLAIM that mutations have no role in adaptive evolution is WRONG.

No one in this thread has said that nutrients and pheromones and RNA balance don't have a role, but it has been shown that MUTATIONS ALSO HAVE A ROLE.

Q.E.D.

http://www.ncbi.n...mutation selection&btnG=&hl=en&as_sdt=0%2C50

You should seek treatment for your pathological lying, James.

phys.org doesn't seem to like pluses. Anyway... Look up mutation and selection on the proper search engines and bask in the many hundreds of thousands of articles on the topic.

http://www.ncbi.nlm.nih.gov/pubmed/?term=mutation selection&btnG=&hl=en&as_sdt=0%2C50

You should seek treatment for your pathological lying, James.

phys.org doesn't seem to like pluses. Anyway... Look up mutation and selection on the proper search engines and bask in the many hundreds of thousands of articles on the topic.

What would be the point? You're attempting to compare ridiculous theory (Statistical Inference) to the biological fact that adaptive evolution is nutrient-dependent and pheromone-controlled. Inferred Natural Selection is not Natural. Food selection and mate selection are natural.

What would be the point?

Yeah, looking at the vast amounts of evidence stacked against you would be far too inconvenient for your deluded worldview. Denying mutation and selection factors besides sexual selection would get you laughed out of any legitimate academic circles. You should try to present at something like the Evolutionary Biology Meeting at Marseilles. I'd pay to see that.

You should try to present at something like the Evolutionary Biology Meeting at Marseilles. I'd pay to see that.

From what I can see, my model already incorporates everything on the agenda:
•Evolutionary biology concepts and modeling;
•Biodiversity and Systematics;
•Comparative genomics ans post-genomics (at all taxomic levels);
•Functional phylogeny;
•Environment and biological evolution;
•Origin of life and exobiology;
•Non-adaptative versus adaptative evolution;
•The "minor" phyla: their usefulness in evolutionary biology knowledge;
What is it that you think is missing from my model or that is not also detailed in my published works? If mutations theory is the only thing missing, that's because it's the most riduculous theory I can imagine. Perhaps if you attend you may learn something about the basic principles of biology and levels of biological organization required to link sensory input directly to behavior in species from microbes to man.

Look up mutation and selection on the proper search engines and bask in the many hundreds of thousands of articles on the topic.

What would be the point? You're attempting to compare ridiculous theory (Statistical Inference) to the biological fact that adaptive evolution is nutrient-dependent and pheromone-controlled. Inferred Natural Selection is not Natural.

Sickle cell mutations are an example of a mutation that is SELECTED FOR in adaptive evolution when malaria is prevalent.
You have tried to argue against this example and have FAILED.
Therefore you calling the involvement of mutations in adaptive evolution a 'ridiculous theory' shows that you are not willing to face the facts.

What is it that you think is missing from my model or that is not also detailed in my published works? If mutations theory is the only thing missing, that's because it's the most riduculous theory I can imagine.

If you find something that nature does 'ridiculous', it reflects poorly on your understanding of nature. As has been shown in this thread, nature uses mutations in adaptive evolution, and your finding it ridiculous doesn't stop nature from doing it.

You call yourself a scientist, yet you fail to update your theory when contradictions to it are shown.

If you update your model to include mutations, I'll take a look at the rest of your model to see if anything else obvious is missing.

If you update your model to include mutations, I'll take a look at the rest of your model to see if anything else obvious is missing.

If you tell me HOW the sickle cell mutation CAUSES adaptive evolution (e.g., by enabling behavior that allows the mutation to be selected and behavior that ensures it is epistatically conserved in some members of one species: ours), I might consider you to be less ignorant than you have repeatedly indicated you are. However, the odds are against anyone else giving you credit for the minimal intelligence that might otherwise be attributed to any anonymous participant who continues to ignore the basic principles of biology and levels of biological organization required to link sensory input to genes, behavior, and back.

It has repeatedly been pointed out to you that mutations CONTRIBUTE to adaptive evolution rather than CAUSING it.

If you are truly ignorant of sickle-cell mutations and why they are selected FOR in malaria-prone areas until they reach a certain percentage of the gene pool, here is an article to start with: http://www.nature...-8756219

As for the behavior that it enables, it has already been pointed out that SURVIVING enables a variety of behaviors, including getting food (for oneself and one's offspring).

Do you now agree that natural selection can select FOR mutations?

If you tell me HOW the sickle cell mutation CAUSES adaptive evolution (e.g., by enabling behavior that allows the mutation to be selected

It is common sense that surviving long enough to mate is beneficial.

One African child dies every minute from Malaria. OBVIOUSLY, they're not going to produce offspring. Being heterogenous for the sickle cell allele limits the life cycle of RBCs enough that the parasite can't grow as well, limiting the effects of it, which increases the fitness of the host, which would give them a better chance to reach maturity.

Resistance to a disease that prevents an organism from mating by killing it before it reaches maturity is obviously going to be selected for. This should be crystal clear.

It has repeatedly been pointed out to you that mutations CONTRIBUTE to adaptive evolution rather than CAUSING it.

Do you now agree that natural selection can select FOR mutations?

No. Is there a model for that? In my model, selection is for nutrient chemicals that metabolize to pheromones and control reproduction. Thus, epigenetic effects of sensory stimuli are directly linked to genetically predisposed behaviors essential for nutrient acquisition and reproduction, which are essential to adaptive evolution. Mutations are selected against. Why don't you tell us all how the sickle cell trait is selected, since you and the other fool here think that mutations CONTRIBUTE to adaptive evolution?

Resistance to a disease that prevents an organism from mating by killing it before it reaches maturity is obviously going to be selected for. This should be crystal clear.

Please clarify HOW organisms select for resistance to disease (e.g., before they are killed). Is there a model for that?

Do you now agree that natural selection can select FOR mutations?

No.

So you are ignoring the selection of sickle-cell mutations because that doesn't fit your theory...

Please clarify HOW organisms select for resistance to disease (e.g., before they are killed). Is there a model for that?

Did you fail to READ or fail to UNDERSTAND the link that I posted?

In case you really don't understand natural selection I'll explain using the sickle-cell example:
The organisms DON'T select for resistance - selection is done TO the organism population. A given organism either has zero copies of the mutation and is likely to die from malaria, has one copy of the mutation and has significant resistance to malaria while not having significant sickle-cell disease, or has two copies and is highly resistant to malaria but is likely to die from sickle-cell disease instead.

So you are ignoring the selection of sickle-cell mutations because that doesn't fit your theory....

No, I'm ignoring your example because there is no model for that. You have somehow managed to conflate theory with adaptive evolution, which is nutrient-dependent and pheromone-controlled in species from microbes to man. That's what I modeled in my published work, which you continue to ignore.

In case you really don't understand natural selection I'll explain using the sickle-cell example:
The organisms DON'T select for resistance - selection is done TO the organism population. A given organism either has zero copies of the mutation and is likely to die from malaria, has one copy of the mutation and has significant resistance to malaria while not having significant sickle-cell disease, or has two copies and is highly resistant to malaria but is likely to die from sickle-cell disease instead.

Is there a model for that?

How do you define model? How is everything from Darwin's finches to antibiotic resistance evolution not a model for mutation and selection?

No, I'm ignoring your example because there is no model for that.

So you ADMIT that you are ignoring a real-world example.

Reality is more important than models, if your model disagrees with reality then YOUR MODEL is wrong.

(And yes, there is a model for sickle cell mutations that even explains the level at which they are maintained in the gene pool - are you seriously ignorant of that?

You have somehow managed to conflate theory with adaptive evolution.

I presented a real-world example. You are the one with a theory, and it has been shown to be incomplete. A true scientist does not ignore a real-world example because it disagrees with his pet theory.

How do you define model? How is everything from Darwin's finches to antibiotic resistance evolution not a model for mutation and selection?

I don't define terms commonly used. Darwin had a theory with no details. I have modeled the mechanisms that link the common molecular biology of microbes to man. Antibiotic resistance occurs via epigenetic effects on alternative splicings that enable the observed species diversity from the bottom-up and top-down as exemplified in the honeybee model organism and other model organisms. Focus on sickle cell is typical -- as a result of thoroughly ingrained ignorance of biology and propagation of a ridiculous theory.

Darwin raised pigeons, but observed the beaks of finches. He probably never knew that avian species depend as much on olfactory/pheromonal input for the development of their behavior as any other species. Did he think that nutrients or mutations caused the adaptive evolution of changes in the beaks?

No, I'm ignoring your example because there is no model for that.

RealScience: So you ADMIT that you are ignoring a real-world example.

No, I'm ignoring your example because there is no model for that.

RealScience: Reality is more important than models, if your model disagrees with reality then YOUR MODEL is wrong.

JVK: My model of genetically predisposed epigenetically effected cause is reality, you idiot. Adaptive evolution is nutrient-dependent and pheromone-controlled, no matter what you think is a real-world example. However, you are a great real-world example of an idiot evolutionary theorist. Thanks for that!

RealScience: So you ADMIT that you are ignoring a real-world example.

No, I'm ignoring your example because there is no model for that.

That YOU have no model for it makes no difference - natural selection will continue to utilize mutations whether your model includes them or not.

JVK: My model of genetically predisposed epigenetically effected cause is reality, you idiot.

No one in this thread has argued against epigenetics being PART of the picture. However since your model does not include a role for mutations, and since mutations have been shown to have a role in adaptive evolution, your model is INCOMPLETE.

...what you think is a real-world example

So state one or more scientific reason why it isn't a valid, or else admit that it is.

I have modeled the mechanisms that link the common molecular biology of microbes to man. Antibiotic resistance occurs via epigenetic effects on alternative splicings

No. Antibiotic resistance occurs AT THE GENETIC LEVEL, not the epigenetic level. We have identified GENOMIC MUTATIONS in coding regions that result in new phenotypes, including resistance.

The variant that leads to sickle cell is a genomic mutation. It has nothing to do with epigenetics. These are facts.

Vernon Ingram demonstrated that the only structural difference between normal adult hemoglobin and sickle-cell hemoglobin is the replacement of glutamic acid with valine in the β-globin amino acid chain (Ingram, 1957; 1959). At the DNA level, this corresponds to a single base change, from adenine to thymine, within the sixth codon (Marotta et al., 1977).

FACT

How willfully ignorant do you have to be to not see this?

I have modeled the mechanisms that link the common molecular biology of microbes to man. Antibiotic resistance occurs via epigenetic effects on alternative splicings

No. Antibiotic resistance occurs AT THE GENETIC LEVEL, not the epigenetic level. We have identified GENOMIC MUTATIONS in coding regions that result in new phenotypes, including resistance.

Who's WE? You seem unfamiliar with the concept of epigenetic effects on alternative splicings that enable selection for genetically predisposed alternative phenotypes and enable the adaptive evolution required for controlled species divergence (as occurs at the advent of sexual differentiation in microbes). See: Diamond, Binstock and JV Kohl (1996) -- the section on molecular epigenetics: "Small intranuclear proteins also participate in generating alternative splicing techniques of pre-mRNA and, by this mechanism, contribute to sexual differentiation..."
Who do you think you are debating here, you ignorant college student?

Who do you think you are debating here...?

"By screening approximately 35,000 possible mutual interactions among Vibrionaceae isolates from the ocean, we show that genotypic clusters known to have cohesive habitat association also act as units in terms of antibiotic production and resistance. Genetic analyses show that within populations, broad-range antibiotics are produced by few genotypes, whereas all others are resistant, suggesting cooperation between conspecifics. Natural antibiotics may thus mediate competition between populations rather than solely increase the success of individuals." http://www.scienc...abstract

Cooperation between conspecifics is nutrient-dependent and pheromone-controlled as is all of adaptive evolution. Only foolish theorists, atheists, and agnostics cling to their theory of mutations as if it actually had ever explained anything of importance to scientific progress. Is Richard Dawkins your hero?

More ad hominems, huh? Real original. Oh look, documented point mutations that result in resistance-

http://www.ncbi.n...19656662

http://www.plospa....1002359

http://mbio.asm.o...00187-11

Only foolish theorists, atheists, and agnostics

What does religion have to do with this?

Antibiotic resistance occurs AT THE GENETIC LEVEL, not the epigenetic level.

@aroc91: Yes, antibiotic resistance has been shown to arise from mutations at the genetic level (which JVK misses due to his narrow view).
But don't fall into a narrow view the other way - that SOME antibiotic resistance arises through mutations does not mean that there are not other cases where antibiotic resistance arises through epigenetic effects on splicing.

Epigenetics are still vastly underestimated by mainstream biologists (although much less so now than a few decades ago), and it would be surprising if there were no cases where an antibiotic triggers an epigentic effect that alters splicing in a way that counteracts the antibiotic.

Cooperation between conspecifics is nutrient-dependent and pheromone-controlled as is all of adaptive evolution. Only foolish theorists, atheists, and agnostics cling to their theory of mutations...

@JVK - That's your THEORY.
Since you say ALL, even a single counter example proves you wrong.
And several counter examples have been presented, and you have failed to come up with any argument against them except that you are ignoring them.

So YOU are the one clinging to a THEORY that has been shown BY REAL-WORLD EXAMPLES to be INCOMPLETE, and repeating statements that have been shown BY REAL-WORLD EXAMPLES to be FALSE.

True. I'm not discounting epigenetics and splicing as a means of granting a population variety, but I have yet to find a case where splicing was responsible for antibiotic resistance.

@aroc - I also haven't seen alternative splicing, especially in response to antibiotics, produce antibiotic resistance. But I also haven't looked, and it would be a useful trait, and given the billions-of-years evolutionary arms race between microbes and antibiotics from other microbes, I would be surprised if it hadn't evolved.

Only foolish theorists, atheists, and agnostics (JVK)

What does religion have to do with this? (aroc91)

If anything religion should make JVK sure that natural selection would utilize mutations if mutations occur. After all, if our simple human-designed genetic algorithms can utilize mutations to drive evolution, surely a system designed by a vastly-superior god could utilize mutations. JVK actually insults his god by thinking that his god can't do something that humans can do.

Who do you think you are debating here...

@JVK - we are obviously debating someone so arrogant that he thinks he can order god to throw away perfectly usable mutations, and then so willfully blind as to ignore that natural selection DOES use them.
But it isn't much of a debate - you have been shown to be wrong, and your model has been shown to be incomplete.

Test JVK's pet theory.
Bring adaptive evolution to standstill.
Control epigenetic effects of nutrients and pheromones to a point where adaptive evolution is suspended in time.

How many times do I need to mention that the honeybee is the MODEL organism for my MODEL; that the MODEL is not a theory; and that the MODEL is also exemplified in species from microbes to man? You boys are either too ignorant to fact check what I'm saying or simply don't want to admit that whatever theory you hold most dear is one that's so unsupported that is has nothing to do with scientific progress during the past several decades, and nothing to do with adaptive evolution.

True. I'm not discounting epigenetics and splicing as a means of granting a population variety, but I have yet to find a case where splicing was responsible for antibiotic resistance.

Would you like alternative splicing to be responsible for some variety but mutations for other variety associated with adaptive evolution? If so, what part of species diversification is caused by mutations? Is there a model for that?

How does what's currently known about the molecular epigenetics of alternative splicing suggest that it is not the cause of antibiotic resistance?

Do you plan to ever express an intelligent thought here?

@aroc - I also haven't seen.... But I also haven't looked... and given the billions-of-years evolutionary arms race between microbes and antibiotics from other microbes, I would be surprised if it hadn't evolved.

I don't think you can "look at" and "see" what happened during what you think is billions-of-years of an evolutionary arms race. However, I can look at a pattern of minimum inhibitory concentrations (MIC) and see what antibiotic is most likely to kill the bacteria that's growing on the media in front of me. I have an advantage: I know that colony growth is nutrient-dependent and pheromone-controlled as is all of adaptive evolution. That advantage allows me to report results that may save an adaptively evolved human life now, not billions of years from now.

The difference between you and me may be your belief in theory vs fact, or it may be that you're an idiot who cannot comprehend the reality of cause and effect I incorporate into results each work-day.

Only foolish theorists, atheists, and agnostics...(JVK)

What does religion have to do with this?(aroc91)

It enables some to embrace the complexity of the cell (i.e., in fact), while others are trying to grasp the complexity of the cosmos (i.e., in theory).

If anything religion should make JVK sure that natural selection would utilize mutations if mutations occur.

Is there a model for that?

Who do you think you are debating here...

@JVK - we are obviously debating someone so arrogant...

I'm informed. You're simply so simple-minded that you perceive me to be arrogant. However, even if you informed yourself you would probably still be an idiot.

How does what's currently known about the molecular epigenetics of alternative splicing suggest that it is not the cause of antibiotic resistance?

The papers I have provided you have shown point mutations resulting in codon changes resulting in amino acid changes resulting in protein structure changes that alter the way those proteins are affected by antibiotics, not alternative splicing.

The single base changes and the protein structure changes that result from them have been identified.

base change =/= alternative splicing

Not sure how to convey this more clearly.

It enables some to embrace the complexity of the cell (i.e., in fact), while others are trying to grasp the complexity of the cosmos (i.e., in theory).

Non sequitur

How does what's currently known about the molecular epigenetics of alternative splicing suggest that it is not the cause of antibiotic resistance?

The papers I have provided you have shown point mutations resulting in codon changes resulting in amino acid changes resulting in protein structure changes that alter the way those proteins are affected by antibiotics, not alternative splicing.

I'm not interested in reading about point mutations as cause. There is no model for that! Where do the amino acids come from?

The single base changes and the protein structure changes that result from them have been identified.

And their role in adaptive evolution is still magical.

Not sure how to convey this more clearly.

Place it in the context of a model of adaptive evolution. You're doing the same thing as you did with the moth example. Focus on one piece of a puzzle in one species, and you go nowhere. Is that your intent?

The papers I have provided you have shown point mutations resulting in codon changes resulting in amino acid changes resulting in protein structure changes that alter the way those proteins are affected by antibiotics, not alternative splicing.

"In Drosophila, recent studies have further suggested that a large fraction of noncoding DNA divergence observed between species may be the product of recurrent adaptive substitution. Similar studies in humans have revealed a more complex pattern, with signatures of recurrent positive selection being largely concentrated in conserved noncoding DNA elements."
http://www.ncbi.n...22399458

Tell us how you get from codon changes resulting in amino acid changes in microbes to nutrient selection, control of reproduction and immune system function in insect species. What does adaptive substitution mean to you? Is it a MUTATION -- in your ridiculous theory?

I'm not interested in reading about point mutations as cause. There is no model for that!

Which trumps observation how?

http://www.iecn.u...lia3.pdf

How's this?

Where do the amino acids come from?

What do you mean by this?

And their role in adaptive evolution is still magical.

Under selective pressures, individuals without advantageous traits aren't as fit. Physical traits are just as important to survival and reproduction as sexual selection. A susceptible bacteria's lineage dies out in the presence of antibiotics.

Place it in the context of a model of adaptive evolution. You're doing the same thing as you did with the moth example. Focus on one piece of a puzzle in one species, and you go nowhere. Is that your intent?

My intent is to get you to understand selective processes besides pheromone-driven sexual selection. These are biology 101 concepts.

"In Drosophila, recent studies have further suggested that a large fraction of noncoding DNA divergence observed between species may be the product of recurrent adaptive substitution. Similar studies in humans have revealed a more complex pattern, with signatures of recurrent positive selection being largely concentrated in conserved noncoding DNA elements."
http://www.ncbi.n...22399458

Tell us how you get from codon changes resulting in amino acid changes in microbes to nutrient selection, control of reproduction and immune system function in insect species. What does adaptive substitution mean to you? Is it a MUTATION -- in your ridiculous theory?

A very similar paper with full text access-

http://www.geneti...949.full

Search for "mutation" and let me know what you find.

JVK

Place it in the context of a model of adaptive evolution. You're doing the same thing as you did with the moth example... Is that your intent?

aroc91:

My intent is to get you to understand selective processes besides pheromone-driven sexual selection. These are biology 101 concepts.

Nutrient-dependent pheromone-controlled adaptive evolution is the concept; you continue to argue from what you know about a ridiculous theory.

For example: "the similarity between the distributions of endemic malaria and those of the thalassemias and sickle cell anemia led to the hypothesis that disease carriers were at a selective advantage where falciparum malaria was common (13, 14). More recent studies of candidate genes support roles for selection on energy metabolism (15), sodium homeostasis (16, 17), and the ability to digest lactose from milk (18, 19) and starch from plants (20)."
Recent studies are the issue here, not ridiculous mutations theory. Educate yourself!

Re: "the similarity between the distributions of endemic malaria and those of the thalassemias and sickle cell anemia... More recent studies of candidate genes support roles for selection on energy metabolism...and the ability to digest lactose from milk and starch from plants(20)."

Mutations theory was disposed of via studies that attest to nutrient-dependent pheromone-controlled adaptive evolution (and by my model). Today's students appear to be taught about a ridiculously outdated theoretical approach.

Anyone who has watched this discussion might now be able to help the next generation learn about adaptive evolution in the correct context of ecological, social, neurogenic, and socio-cognitive niche construction. Someday, students must take a realistic approach to understanding adaptive evolution, instead of arguing from a ridiculous theory. Help them move forward if you can. I need to focus on making more scientific progress.

For example: "the similarity between the distributions of endemic malaria and those of the thalassemias and sickle cell anemia led to the hypothesis that disease carriers were at a selective advantage where falciparum malaria was common (13, 14). More recent studies of candidate genes support roles for selection on energy metabolism (15), sodium homeostasis (16, 17), and the ability to digest lactose from milk (18, 19) and starch from plants (20)."
Recent studies are the issue here, not ridiculous mutations theory. Educate yourself!

From that same study:

"Our results extend upon and are complementary to results of previous scans for natural selection in humans"

They even reference the paper "Natural selection has driven population differentiation in modern humans".

That's exhibited in the part where they talk about adaptation to cold environments-r esistance to cold temperature.

@JVK - Anyone who has watched this discussion will see that you have provided NO evidence to support your statements that mutations play no role in adaptive evolution, and that you have FAILED to provided a counter-argument when presented a REAL-WORLD example that contradicts your statement.

Someday you may take a realistic approach to understanding adaptive evolution, instead of dismissing reality when reality doesn't match your theory.

Rather than trying to defend an aspect of your theory, you should update your theory based on reality.

I try to help everyone move forward, including you.

Molecular evolutionary analyses of insect societies http://www.pnas.o...abstract
Here it is again (above): evidence of nutrient-dependent pheromone-controlled adaptive evolution sans mutations in the invertebrate model that is based on our representation of the mammalian model of hormone-organized and hormone-activated behavior (1996).

@JVK - Anyone who has watched this discussion will see that you have provided NO evidence to support your statements that mutations play no role in adaptive evolution...

That's because I'm not the one who said mutations play a role in adaptive evolution. I said they didn't; there is no evidence that they do; and no model suggests they do. Only an idiot would continue to say I need to provide evidence that mutations don't play a role, without telling us what role they play in either Natural Selection (i.e., for WHAT?) or in Sexual Selection (for WHAT?). Clearly, you are that idiot.

From that same study:

"Our results extend upon and are complementary to results of previous scans for natural selection in humans"

They even reference the paper "Natural selection has driven population differentiation in modern humans".

Natural selection for WHAT? You're not very bright, are you?

without telling us what role they play in either Natural Selection (i.e., for WHAT?)

You have been told what role, repeatedly. For example, it has been pointed out that sickle cell mutations are selected FOR in areas where malaria is prevalent, which shows your statement to be WRONG (and your theory to be incomplete). So for you to say that there is no evidence is willful ignorance on your part.

No matter how you much cover your eyes and say that mutations play no role in adaptive evolution, natural selection will keep on using them.

Would you like alternative splicing to be responsible for some variety but mutations for other variety associated with adaptive evolution?

It does not matter what we would like - what matters is what natural selection actually does.
Mutations are responsible for variations in gene sequences. Some mutations are point changes (SNPs), some are much bigger (reversals, duplications, deletions, chromosomes splitting and joining). Some affect transcription, some affect proteins produced, some affect RNAs produced.

Epigenetic changes are changes to the accessiblity of the genes, and strongly affect transcription and thus RNAs.

RNAs are the main computational engines of the cell, managing which proteins are produced at which times.

All play roles in evolution through natural selection.

Would you like alternative splicing to be responsible for some variety but mutations for other variety associated with adaptive evolution?

It does not matter what we would like - what matters is what natural selection actually does.
Mutations are responsible for variations in gene sequences. Some mutations are point changes (SNPs), some are much bigger (reversals, duplications, deletions, chromosomes splitting and joining). Some affect transcription, some affect proteins produced, some affect RNAs produced.

Epigenetic changes are changes to the accessiblity of the genes, and strongly affect transcription and thus RNAs.

RNAs are the main computational engines of the cell, managing which proteins are produced at which times.

All play roles in evolution through natural selection.

Is there a model for that?

That's because I'm not the one who said mutations play a role in adaptive evolution. I said they didn't; there is no evidence that they do; and no model suggests they do.

Here's a model- http://www.iecn.u...lia3.pdf

and I have provided you with the evidence repeatedly, from the mutations responsible for masking moths, resulting in the differential predation to mutations resulting in antibiotic resistance. There is a ton of research that shows how mutations to genes of antibiotic-targeted proteins produce structural changes that prevent them from binding, making the bacteria that possess those mutations more successful in the presence of those antibiotics, leading to a resistant population.

The environment ultimately determines the relative success of a mutation.

either Natural Selection (i.e., for WHAT?)

See above.

or in Sexual Selection (for WHAT?)

I never denied pheromone involvement in mate selection, but there are other factors besides that.

I've already shown you the mutations responsible for new phenotypes and the population bottlenecks that follow the predation and antibiotic natural selection that explain the new-found dominance of those advantageous traits.

As I've said before, success of a species is reliant on finding food, mating, and surviving in the first place to do both of those things.

Is there a model for that?

@JVK - You have already been presented examples, such as sickle-cell mutations. If you truly have any experience in the field, you will know that that sickle-cell mutations have been well modeled, and that the models even even explaining the frequency to which the mutations accumulate relative to the prevalence of malaria.

You ignore both the models AND that such mutations happen and are selected for in the real world because they conflict with your preconceived ideas. But nature doesn't stop using mutations because your model doesn't include them or because you ignore models that do.

Here's a model- http://www.iecn.u...lia3.pdf

I guess that means this is the proof of the hidden genetic code:

"Using the Markov property at time 1 and Lemmas 5.4 and 5.5, we can prove that,when we replace Sn by the n-th mutation time of XK
t/KuK and Yt by the support of XK t/KuK (when it is a singleton) in the LHS of (5.16) and (5.17), the same relations hold in the
limit K ! 1. Therefore, Theorem 5.1 is proved for one-dimensional time marginals."

It could also be proof that you are an idiot theorist who does not understand ligand-receptor binding or anything else about the basic principles of biology or levels of biological organization required to link sensory cause to epigenetic effects on adaptive evolution. Please tell us, what do you think Theorem 5.1 proves?

Is there a model for that?

@JVK - You have already been presented examples, such as sickle-cell mutations. If you truly have any experience in the field, you will know that that sickle-cell mutations have been well modeled, and that the models even even explaining the frequency to which the mutations accumulate relative to the prevalence of malaria.

What part of "selection on energy metabolism" (see below) do you not understand in the context of sickle cell "mutation" vs nutrient-dependent pheromone-controlled?

"the similarity between the distributions of endemic malaria and those of the thalassemias and sickle cell anemia led to the hypothesis that disease carriers were at a selective advantage where falciparum malaria was common (13, 14). More recent studies of candidate genes support roles for selection on energy metabolism (15), sodium homeostasis (16, 17), and the ability to digest lactose from milk (18, 19) and starch from plants (20)."

either Natural Selection (i.e., for WHAT?)

or in Sexual Selection (for WHAT?)

THEORIST: I never denied pheromone involvement in mate selection, but there are other factors besides that.

JVK: Tell us how the other factors cause or contribute to the required ecological, social, neurogenic, and socio-cognitive niche construction enabled by nutrient-dependent pheromone-controlled adaptive evolution.

THEORIST: I've already shown you the mutations responsible for new phenotypes and the population bottlenecks that follow the predation and antibiotic natural selection that explain the new-found dominance of those advantageous traits.

JVK: How does any mutation promote:

...finding food, mating, and surviving in the first place to do both of those things.

What part of "selection on energy metabolism" (see below) do you not understand in the context of sickle cell "mutation" vs nutrient-dependent pheromone-controlled?

The part where you continue to deny any selection for mutations in spite of real-world examples such as sickle-cell mutations.

As for energy metabolism I pointed out many posts ago that sickle cell mutations are selected FOR where malaria is prevalent in spite of it interfering with oxygen metabolism. What part of that did YOU fail to comprehend.

THEORIST: There is no model for mutations having a role in adaptive evolution.

SCIENTISTS: Here are real-world examples of mutations being selected for in adaptive evolution: (numerous examples provided)

THEORIST: I can ignore that because there is no model for it.

SCIENTISTS: It is well modeled, and the models even produce the observed allele frequency distribution.

THEORIST: I ignore the model because it is ridiculous. So there is no model because I ignore it.

SCIENTISTS: That you ignore the model doesn't make it not exist, and that you ignore the role of mutations doesn't make nature stop using them.

THEORIST degrades into endless repetition in an infinite loop of denial of reality punctuated by insults that apply to himself.

JVK:

How does any mutation promote: ...finding food, mating, and surviving in the first place to do both of those things.

Did you fail to read the paper on sickle cell mutations, or fail to comprehend it?
Here it is again: http://www.nature...-8756219

JVK:

How does any mutation promote...

Did you fail to read the paper on sickle cell mutations, or fail to comprehend it?
Here it is again: http://www.nature...-8756219

"He reasoned that possession of a single mutant gene must confer a survival advantage and be positively selected at the population level."

Adaptive evolution occurs via selection of nutrients and their metabolism to pheromones that signal reproductive fitness so that nutrient-dependent pheromone-controlled reproduction ensures survival of the species. Selection does not occur for mutations at the population level; there are no molecular mechanisms.

Reproductive isolation can arise with little or no morphological differentiation http://www.scienc...64.short That means mutations associated with visual input are not selected, and that you are an idiot with no future in scientific pursuits. Keep your job at Burger King!

JVK:"He reasoned that possession of a single mutant gene must confer a survival advantage and be positively selected at the population level."

Yes, that was the theory proposed in 1954. But you missed the next 50 years, as summarized in the paper:

"Allison and others used epidemiological, statistical, and experimental methods to prove an association between sickle-cell trait and malaria resistance (Allison, 2004).

"... among children in the intermediate age window, a lower percentage of those with sickle-cell trait get cerebral malaria, severe malarial anemia, or other lethal consequences, and on average, the number of parasites in their bloodstream is decreased (Aidoo et al., 2002). These subtle differences mean that more individuals with the trait survive to reach reproductive age and pass on the mutant gene to their offspring."

So your claim that

Selection does not occur for mutations at the population level

is WRONG.

Reproductive isolation can arise with little or no morphological differentiation http://www.scienc...64.short That means mutations associated with visual input are not selected.

That just goes to show how absurd your reasoning on mutations is.
First, that reproductive isolation CAN arise without a change in what a mate looks like does NOT imply that that is the ONLY way isolation can arise. There are so many examples of diverging species having different appearance that to find ones that were morphologically the same was worthy of a paper!
Second, visual input can be selected for things other than being attracted to a different look of a potential mate. Improved eyesight can also help find food or avoid predators, for example.