Gene Involved in Brain Development Evolved Rapidly in Humans

[mark kennedy]

My answer is the same as it would be for any other trait: random mutation + differential reproductive success.

You forget or never realized that the researchers said 1 or 0 nucleotides could be accounted for by chance. Did you bother to even read up on the specifics of the genes spoken of in the article linked in the OP? Because you don't seem to comprehend the magnitude of an 18 nucleotide sequence in a gene 118 nucleotides long. Particularly when it is involved in the development of the neocortex in a highly conserved area.

If you don't think the interaction of those elements can produce the human brain, you are welcome to explain why. Finding different ways to say "because they can't" isn't an argument.

Saying that it would be benefical isn't an answer either. Why are you avoiding the implications of your own source material and the specifics of the topic you started?

This is just insulting. Show me where it has been published that the HAR1 gene changes can't be accounted for by existing mechanisms.

Again you are talking in generalities when the specifics are readily available. The Har1 gene is highly conserved and only encounterd a two nucleotide polymorphism in 60 million years of evolution. Then in a fraction of that time accumulated 18 nucleotides that come to 6 completly new amino acid sequences. Random mutations are not an explanation and the researchers explicitly said that in no uncertain terms.

Is this some Behe-esque "the evolutionary explanation must explicitly account for the precise location and behavior of every molecule before I consider it valid" rhetoric? Because I'm tired of wasting my time on nonsense.

For someone tired of rhetoric you are not shy about basing your entire argument on it. So what was the mechanism? You say, natural selection due to a benefical effect but never explain how the change occured in the first place.

Show me where it says that the changes can't have happened via evolutionary mechanisms.

You mean the rhetoric of natural selection, that is not an evolutionary mechanism it's circular logic. It was preserved because it was benefical, nevermind that this gene is highly conserved and random mutations have been selected against for 60 million years.

It's utterly mind-boggling that you think you can mine support for your position by quoting evolution-supporters out of context. Stop doing it.

Now you are complaining about a discussion of the source material you proposed in the OP. You don't have an answer for how the gene was altered and the one lame attempt was contradicted by the researchers themselves. Random mutations explain 0 or 1 substitutions, not 18 in a highly conserved, vital region.

I want you to say something other than a variation of "big brain = impossible to evolve."

I want you to say something besides natural selection responded to a beneficial effect. An effect that you offer no viable cause for and lack any substantive or relevant source material beyond an article you now object to being quoted.

Keep talking in circles, I really get a kick out of it when evolutionists can't answer with anything but generalities.

 

[Chalnoth]

Again you are talking in generalities when the specifics are readily available. The Har1 gene is highly conserved and only encounterd a two nucleotide polymorphism in 60 million years of evolution. Then in a fraction of that time accumulated 18 nucleotides that come to 6 completly new amino acid sequences. Random mutations are not an explanation and the researchers explicitly said that in no uncertain terms.

What researchers? Where?

 

[TeddyKGB]

You forget or never realized that the researchers said 1 or 0 nucleotides could be accounted for by chance. Did you bother to even read up on the specifics of the genes spoken of in the article linked in the OP? Because you don't seem to comprehend the magnitude of an 18 nucleotide sequence in a gene 118 nucleotides long. Particularly when it is involved in the development of the neocortex in a highly conserved area.

The implication here is that 18 beneficial mutations could not have occurred in that gene.

Now is the time for you to stop saying it and start demonstrating it.

Saying that it would be benefical isn't an answer either. Why are you avoiding the implications of your own source material and the specifics of the topic you started?

Show me where any of the researchers quoted thus far are skeptical of the ability of evolution to produce the changes in the gene in question.

Show me. Stop telling me that something is obviously the case and show me that it is the case.

Again you are talking in generalities when the specifics are readily available. The Har1 gene is highly conserved and only encounterd a two nucleotide polymorphism in 60 million years of evolution. Then in a fraction of that time accumulated 18 nucleotides that come to 6 completly new amino acid sequences. Random mutations are not an explanation and the researchers explicitly said that in no uncertain terms.

They did not say that. What they said was that given the conserved natures of related genes, and the gene differences between other animals, only one or two mutations would be expected.

They did not say that mutations and selection could not account for the changes.

For someone tired of rhetoric you are not shy about basing your entire argument on it. So what was the mechanism? You say, natural selection due to a benefical effect but never explain how the change occured in the first place.

What in the bloody heck are you talking about?

You mean the rhetoric of natural selection, that is not an evolutionary mechanism it's circular logic. It was preserved because it was benefical, nevermind that this gene is highly conserved and random mutations have been selected against for 60 million years.

Oh, please don't give me the "circular logic" tripe. That's Hovind-level stuff. Don't go there.

Now you are complaining about a discussion of the source material you proposed in the OP. You don't have an answer for how the gene was altered and the one lame attempt was contradicted by the researchers themselves. Random mutations explain 0 or 1 substitutions, not 18 in a highly conserved, vital region.

Read it again.

I want you to say something besides natural selection responded to a beneficial effect. An effect that you offer no viable cause for and lack any substantive or relevant source material beyond an article you now object to being quoted.

Keep talking in circles, I really get a kick out of it when evolutionists can't answer with anything but generalities.

I knew you'd pull this stunt.

Evolution is not harmed by an inability to provide a moment-by-moment recount of gene change or selection.

 

[mark kennedy]

What researchers? Where?

This is the abstract from a recent paper that Teddy heard about in a news article.

"We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these 'human accelerated regions', HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal-Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal-Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology."

(An RNA gene expressed during cortical development evolved rapidly in humans. Nature 2006)

Here is a brief but very good discussion of the research.

http://www.johnhawks.net/weblog/index.html?find=HAR1&plugin=find&path=

 

[mark kennedy]

The implication here is that 18 beneficial mutations could not have occurred in that gene.

You really have no idea what is involved do you? Only 2 substitutions between a chimpanzee and a chicken in 60 million years. It plays a crucial role in the development of the neurons in the developing human neocortex from 7 to 19 gestational weeks. You have two choices here, relaxed functional constraint or positive selection. For there to be positive selection you need 6 amino acids substituted. Random mutations could not possible begin to account for this, changing nucleotides in this sequence is beyond impossible, it's insane.

Now is the time for you to stop saying it and start demonstrating it.

You didn't even read your own source material did you Teddy? Did you?

Show me where any of the researchers quoted thus far are skeptical of the ability of evolution to produce the changes in the gene in question.

You miss the point, you said random mutations plus natural selection was the answer. Random mutations was never considered and in order for there to be positive selection 6 amino acids have to be substituted in a meaningfull way. No one is questioning evolution as long as alleles change in living systems which is another word you are using that you don't understand.

Show me. Stop telling me that something is obviously the case and show me that it is the case.

I did show you and you said random mutations, this highly conserved area could not handle random mutations. That's why it was so highly conserved for 60 million years.

They did not say that. What they said was that given the conserved natures of related genes, and the gene differences between other animals, only one or two mutations would be expected.

You are wrong again because you didn't bother to read or follow up your source material. They said that only 2 nucleotides diverged between chickens and chimpanzees which represents 60 million years of evolution. Chimpanzees as compared to humans diverged by 18 with either 1 or 0 expected by chance (random mutations). You are wrong again because you don't bother to read the source material, such a pointless error is easily avoided.

They did not say that mutations and selection could not account for the changes.

What they said was that relaxed functional constraint is out due to the sensitivity of the area. That leaves only one possibility, positive selection which begs the question of how the alteration occured in the first place. I knew you would say natural selection as if it were this magic word that makes the impossible seem reasonable. You guys allways do.

What in the bloody heck are you talking about?

I'm not talking about evolution or the HAR1f gene, that's for sure. You stubbornly refused to even discuss it even though you challenged me to this discussion.

Oh, please don't give me the "circular logic" tripe. That's Hovind-level stuff. Don't go there.

That is so childish, don't you realize that natural selection means the preservation of a favored trait. It may well account for the survival of the fittest but is no explanation at all for the arrival of the fittest. Your just looking for a clutch phrase and using a very precise scientific tool like a club.

Read it again.

Actually, I'm looking for the paper since all I have is the abstract. You didn't even read the news article so practice what you preach.

I knew you'd pull this stunt.

Yea, you are probably not used to creationists who can read a scientific paper. That is why you don't have to do any reading or research but I do and you should be prepared for that when challenging me to a debate.

Evolution is not harmed by an inability to provide a moment-by-moment recount of gene change or selection.

Evolution as science or evolution as history or evolution as a modern mythology? Let me guess, you don't know the difference right? Because this kind of research is dispelling the myth of common ancestory one nucleotide at a time. You may well conclude a common ancestor after considering the evidence but there is ample reason to reject the a priori assumptions of ill-informed protaganists like yourself.

 

[Chalnoth]

This is the abstract from a recent paper that Teddy heard about in a news article.

"We devised a ranking of regions in the human genome that show significant evolutionary acceleration. Here we report that the most dramatic of these 'human accelerated regions', HAR1, is part of a novel RNA gene (HAR1F) that is expressed specifically in Cajal-Retzius neurons in the developing human neocortex from 7 to 19 gestational weeks, a crucial period for cortical neuron specification and migration. HAR1F is co-expressed with reelin, a product of Cajal-Retzius neurons that is of fundamental importance in specifying the six-layer structure of the human cortex. HAR1 and the other human accelerated regions provide new candidates in the search for uniquely human biology."

(An RNA gene expressed during cortical development evolved rapidly in humans. Nature 2006)

Here is a brief but very good discussion of the research.

http://www.johnhawks.net/weblog/index.html?find=HAR1&plugin=find&path=

They don't say anywhere that the rate of evolution of this gene was, "too fast." They does, of course, note that it is faster than it has been observed to evolve in any other mammal studied. This really doesn't say anything more than the gene was strongly selected-for in our pre-human ancestors, but not any other mammals. I'm sure that there are some involved in the genetics and/or paleontology fields that are very interested in this development, and are investigating the development of this gene as we speak.

 

[TeddyKGB]

You really have no idea what is involved do you? Only 2 substitutions between a chimpanzee and a chicken in 60 million years. It plays a crucial role in the development of the neurons in the developing human neocortex from 7 to 19 gestational weeks. You have two choices here, relaxed functional constraint or positive selection. For there to be positive selection you need 6 amino acids substituted. Random mutations could not possible begin to account for this, changing nucleotides in this sequence is beyond impossible, it's insane.

Still waiting for you to demonstrate this.

You miss the point, you said random mutations plus natural selection was the answer. Random mutations was never considered and in order for there to be positive selection 6 amino acids have to be substituted in a meaningfull way. No one is questioning evolution as long as alleles change in living systems which is another word you are using that you don't understand.

What I don't understand is anything you just wrote.

I did show you and you said random mutations, this highly conserved area could not handle random mutations. That's why it was so highly conserved for 60 million years.

Show, prove, demonstrate, evidence. I don't care, just stop asserting it.

You are wrong again because you didn't bother to read or follow up your source material. They said that only 2 nucleotides diverged between chickens and chimpanzees which represents 60 million years of evolution. Chimpanzees as compared to humans diverged by 18 with either 1 or 0 expected by chance (random mutations). You are wrong again because you don't bother to read the source material, such a pointless error is easily avoided.

I read all that. You still don't understand what they mean when they say "by chance."

What they said was that relaxed functional constraint is out due to the sensitivity of the area. That leaves only one possibility, positive selection which begs the question of how the alteration occured in the first place. I knew you would say natural selection as if it were this magic word that makes the impossible seem reasonable. You guys allways do.

Because natural selection has 150 years of supporting data. If you want to start questioning the whole enterprise, you'll have to provide a reason why.

I'm not talking about evolution or the HAR1f gene, that's for sure. You stubbornly refused to even discuss it even though you challenged me to this discussion.

I need you to acknowledge first that "by chance" does not mean "by random mutation."

That is so childish, don't you realize that natural selection means the preservation of a favored trait. It may well account for the survival of the fittest but is no explanation at all for the arrival of the fittest. Your just looking for a clutch phrase and using a very precise scientific tool like a club.

No, I just don't know why circularity is supposed to be a problem. Does it dispute that some traits will provide a competitive advantage? Does it dispute that traits are heritable?

Evolution as science or evolution as history or evolution as a modern mythology? Let me guess, you don't know the difference right? Because this kind of research is dispelling the myth of common ancestory one nucleotide at a time.

That sounds like something Dembski said in one of your dreams.

You may well conclude a common ancestor after considering the evidence but there is ample reason to reject the a priori assumptions of ill-informed protaganists like yourself.

So we're not allowed to use the massive case for common descent already built? We have to prove it anew every time a creationist challenges the evolution of a particular trait?

I think I'm going to cry.

 

[mark kennedy]

They don't say anywhere that the rate of evolution of this gene was, "too fast." They does, of course, note that it is faster than it has been observed to evolve in any other mammal studied. This really doesn't say anything more than the gene was strongly selected-for in our pre-human ancestors, but not any other mammals. I'm sure that there are some involved in the genetics and/or paleontology fields that are very interested in this development, and are investigating the development of this gene as we speak.

What it says is that what would have been expected was 1 or 0 nucleotides substituted. Instead there were 18 which would be accelerated evolution in a highly conserved area. It is assumed that it was changed and that it was selected for based a benefit but how the changed actually occured is not even guessed at. Evolutionists beg the question of proof in this way, when you come to a node in the Darwinian tree of life you just insert the magic word 'selection' and presto, a transitional form.

 

[mark kennedy]

Still waiting for you to demonstrate this.

I'm still waiting for you to actually read your own source material. You have yet to make a single substantive remark about it and going in circles so fast it's making me dizzy.

What I don't understand is anything you just wrote.

If that isn't a textbook example of an argument from incredulity I don't know what is.

Show, prove, demonstrate, evidence. I don't care, just stop asserting it.

You allready have it and refuse to look at it, in fact you have stubbornly refused to even discuss it. You said something to the order of 'its out of my hands' whatever that means.

I read all that. You still don't understand what they mean when they say "by chance."

Random mutations occur by chance and if in the germline cells the changes can be inherited. Again! the gene was highly conserved for 60 million years and then in the last 1.5 million it gets 18 nucleotide substitutions.

Because natural selection has 150 years of supporting data. If you want to start questioning the whole enterprise, you'll have to provide a reason why.

What I told you is you don't understand the expression you are using. You seem to think natural selection can be used interchangably with evolution, which is absured. Natural selection is the preservation of favored traits but the death of the less fit within specices competing for resources.

I need you to acknowledge first that "by chance" does not mean "by random mutation."

Random (spontaneous) mutations are entirely by chance, usually due to transcript errors. Since you have no clue what I am talking about on the most basic level I suggest you do a little research:

"Causes of mutation Two classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens."

http://en.wikipedia.org/wiki/Mutation

No, I just don't know why circularity is supposed to be a problem. Does it dispute that some traits will provide a competitive advantage? Does it dispute that traits are heritable?

You don't know why circular reasoning is a problem...really? No one is going to dispute that an improve neocortex is an advantage but you are talking about the effect. Once again you have the effect before the cause and still have no clue what is involved here.

That sounds like something Dembski said in one of your dreams.

He did comment on this research but bear in mind this is just the first region explored. What it discovered was a gene that would have had to evolve at an unprecedented level. Mind you, it is not currently evolving which is why begging the question of proof is such a superficial exercise.

"And beyond HAR1 lie HAR2, HAR3, and so on through the 49 regions Pollard identified with her DNA screen. "We've only studied one of these regions carefully," said Haussler. "Now we have to go through the other 48."

http://almostheadline.com/site/AlmostHeadline/8BCDFA29-DE6F-461E-ABC4-C961D6E2040F.html

So we're not allowed to use the massive case for common descent already built? We have to prove it anew every time a creationist challenges the evolution of a particular trait?

Common descent is neither proven nor provable. Arguments are based almost exclusivly on ad hoc conjecture and a priori assumption. You have yet to offer a single possible cause for the effect that was supposed to be selected for.

I think I'm going to cry.

Really? Because I can't stop laughing.

 

[TeddyKGB]

If that isn't a textbook example of an argument from incredulity I don't know what is.

I think you misread your logical fallacies textbook.

You allready have it and refuse to look at it, in fact you have stubbornly refused to even discuss it. You said something to the order of 'its out of my hands' whatever that means.

I don't have to make the case for common descent all over again just to support a single data point.

Random mutations occur by chance and if in the germline cells the changes can be inherited. Again! the gene was highly conserved for 60 million years and then in the last 1.5 million it gets 18 nucleotide substitutions.

I know. Now provide the evidence that those mutations couldn't have accrued via naturalistic evolution.

What I told you is you don't understand the expression you are using. You seem to think natural selection can be used interchangably with evolution, which is absured. Natural selection is the preservation of favored traits but the death of the less fit within specices competing for resources.

Have I denied that mutations are half of the evolutionary picture? If so, where?

Random (spontaneous) mutations are entirely by chance, usually due to transcript errors. Since you have no clue what I am talking about on the most basic level I suggest you do a little research:

"Causes of mutation Two classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens."

http://en.wikipedia.org/wiki/Mutation

I know what random mutations are. But that's not what the researchers in question mean when they say "by chance."

You don't know why circular reasoning is a problem...really? No one is going to dispute that an improve neocortex is an advantage but you are talking about the effect. Once again you have the effect before the cause and still have no clue what is involved here.

I don't know what you're talking about. The proximate causes of evolution are 1) mutations, which provide new traits or change existing ones; and 2) an environment of limited means to reproductive success.

Any time (2) exists, there will necessarily be competition. And any time there is competition, there will necessarily be winners and losers.

He did comment on this research but bear in mind this is just the first region explored. What it discovered was a gene that would have had to evolve at an unprecedented level. Mind you, it is not currently evolving which is why begging the question of proof is such a superficial exercise.

"Not currently evolving"? Are you kidding? You think a microcosm of millions of years of natural selection is a logical request?

"And beyond HAR1 lie HAR2, HAR3, and so on through the 49 regions Pollard identified with her DNA screen. "We've only studied one of these regions carefully," said Haussler. "Now we have to go through the other 48."

http://almostheadline.com/site/AlmostHeadline/8BCDFA29-DE6F-461E-ABC4-C961D6E2040F.html

So. What.

Common descent is neither proven nor provable. Arguments are based almost exclusivly on ad hoc conjecture and a priori assumption. You have yet to offer a single possible cause for the effect that was supposed to be selected for.

Common descent is far, far, far and away the best explanation for the taxonomic nested hierarchies. There is simply no intelligence-invoking model that is not massively ad hoc and question-begging.

Your so-called counterexamples are exceedingly narrow in scope, yet your conclusions are unsupportably broad. The human cortex is three times the size of the chimp cortex, therefore common ancestry is false?

I don't know what to do with you anymore.

 

[mark kennedy]

I think you misread your logical fallacies textbook.

At least I read it before challenging someone to a debate on the subject.

[I don't have to make the case for common descent all over again just to support a single data point.

You don't see the need to make a case for the accelerated evolution of a gene involved in the development of the neocortex. Then you don't have anything because you have no clue why this research is important.

I know. Now provide the evidence that those mutations couldn't have accrued via naturalistic evolution.

Yes I do and you are still oblivious to the implications of this research. You really don't have a single idea what causes 18 nucloetides to be substituted in a highly conserved gene. There is a good reason for that, it's because it simply does not happen.

Have I denied that mutations are half of the evolutionary picture? If so, where?

When you say mutations with regards to evolution do you mean somatic or germline?

I know what random mutations are. But that's not what the researchers in question mean when they say "by chance."

Yes it is.

I don't know what you're talking about. The proximate causes of evolution are 1) mutations, which provide new traits or change existing ones; and 2) an environment of limited means to reproductive success.

Which is why the directly observed and demonstrated evolutionary mechanisms cannot account for the overhaul of such a highly conserved gene. Perhaps you have an example of a known mutation in a gene involved in the development of the human brain resulting in a beneficial effect. Let me save you some time, it does not exist except in the mind of evolutionists.

Any time (2) exists, there will necessarily be competition. And any time there is competition, there will necessarily be winners and losers.

There you go talking about the effect, I'm still waiting for the cause of the change in the nucleotide sequence.

"Not currently evolving"? Are you kidding? You think a microcosm of millions of years of natural selection is a logical request?

The HAR1 gene is not evolving, that is for sure. By the way, I need to make a correction.

"The difference between chickens and chimps - which are separated by 310 million years of evolution - is just two mutations out of a total DNA sequence of 118 "letters" of the genetic code. Yet the difference
between chimps and humans - separated by 6 million years - is 18 mutations in the same DNA region."

http://groups.google.co.uk/group/sc...hread/79f9201e8a10a7cc/5a7da3306c67c9a2?hl=en

I said 60 million years when it was 310 million years of evolution. That is getting back pretty close to the Cambrian explosion. Then, 1.5 Mya it suddenly accumulated 18 substitutions, you have no clue how it happened and neither does anyone else. Mainly because it doesn't happen.

Common descent is far, far, far and away the best explanation for the taxonomic nested hierarchies. There is simply no intelligence-invoking model that is not massively ad hoc and question-begging.

Common descent is a modern mythology, nothing more. No natural mechanism can or does alter vital genes on this level and you are still talking in circles around nothing.

Your so-called counterexamples are exceedingly narrow in scope, yet your conclusions are unsupportably broad. The human cortex is three times the size of the chimp cortex, therefore common ancestry is false?

If it is falsifiable at all, this is the kind of evidence that falsifies it conclusivly. Not one beneficial effect can be demonstrated or even imagined yet this divergance resulting from mutations are assumed a priori. The size and complexity of the human brain must have a natural cause or the LCA of chimpanzees and humans is a mythical creature that did not exist.

I don't know what to do with you anymore.

Try studying the subject before inviting me into a debate. If you want to name me specifically in the OP then you had better be prepared to present a substantive argument. If not then I suggest you use your time sniping as creationists who don't know anything about the subject.

Learn your terminology, study your source material and consider the implications of the accerleated evolution of human specific genes related to the development of the human brain.

Why don't you type 'the effect of mutations on the human brain', you will find something like this most of the time.

"Simply put, evolution has been working very hard to produce us humans," said Bruce Lahn, an assistant professor of human genetics at the University of Chicago and an investigator at the Howard Hughes Medical Institute.

"Our study offers the first genetic evidence that humans occupy a unique position in the tree of life."

By comparing mutations that had no effect on the function of the genes with those mutations that did, they came up with a measure of the pressure of natural selection on those genes.

The scientists found that the human brain's genes had gone through an intense amount of evolution in a short amount of time - a process that far outstripped the evolution of the genes of other animals.

"We've proven that there is a big distinction," Prof Lahn said. "Human evolution is, in fact, a privileged process because it involves a large number of mutations in a large number of genes.

"To accomplish so much in so little evolutionary time - a few tens of millions of years - requires a selective process that is perhaps categorically different from the typical processes of acquiring new biological traits."

http://cogweb.ucla.edu/Abstracts/Dorus_04.html


Learn a little something about the subject before calling me out personally next time.

 

[Chalnoth]

Mark, I'm sorry, but you are still arguing from incredulity. It is still entirely possible for natural selection to have kept that particular gene very constant in all animals previous to humans, all the while allowing for rapid changes in humans.

Why? Well, when there is a mutation, it is unlikely for that mutation to be entirely beneficial. One needs there to be substantial pressure in favor of that mutation for it to lead to a benefit to the organism. This is why organisms just don't evolve very much unless they are currently poorly-suited to their environment.

Now, how hard it is for there to have been a mutation in the HAR1 gene? How infrequently would such a mutation occur? It has been estimated that the rate of mutation in humans will lead to approximately 175 transcription errors with each generation. The HAR1 gene contains 118 base pairs, out of about 3 billion in the human genome.

That's about a 7/1,000,000 chance that each person will be born with a mutation in the HAR1 gene.

If we consider a population of 100,000 early hominids, then one needs only wait 1-2 generations before one of them has a mutation in the HAR1 gene. So we wait, oh, 10-20 generations until one of those mutations is beneficial. If that gene is subject to strong enough selective pressure, that gene will spread rather quickly throughout the population. Not all of the mutations need be sequential, either: beneficial mutation A could combine with beneficial mutation B through breeding rather than one organism starting with mutation A later obtaining mutation B.

In the 20 million years or so since we split off from Chimpanzees, there has been far more than enough time for the merely 18 separate mutations to have occurred. We're talking about something like 1,000,000 generations here! It's not hard to believe at all, to me, that such a change could occur within a few thousand generations.

 

[TeddyKGB]

We are talking past each other on literally every debate point. You already think you know more about the topic than the experts, and you are consistently inferring conclusions from the articles that are simply not supported.

I think at this point you're just contradicting whatever I say, so I'll defer to whomever else wants to engage.

 

[mark kennedy]

Mark, I'm sorry, but you are still arguing from incredulity. It is still entirely possible for natural selection to have kept that particular gene very constant in all animals previous to humans, all the while allowing for rapid changes in humans.

No I am not incredulous in the slightest, you are assuming a change that is unprecedented in 310 million years of evolution.

Why? Well, when there is a mutation, it is unlikely for that mutation to be entirely beneficial. One needs there to be substantial pressure in favor of that mutation for it to lead to a benefit to the organism. This is why organisms just don't evolve very much unless they are currently poorly-suited to their environment.

Organisms adapt to new environments and ecological niches perfectly fine without mutations. Mutations with a beneficial effect are so rare that they don't even have a rate at which they are fixed in species.

Now, how hard it is for there to have been a mutation in the HAR1 gene? How infrequently would such a mutation occur?

There are two nucleotides substituted in 310 million years and then suddenly 18 are substituted. Gradualistic genetic statistics are completly meaningless unless applied toward the accelerated evolution of the genes involved.

It has been estimated that the rate of mutation in humans will lead to approximately 175 transcription errors with each generation. The HAR1 gene contains 118 base pairs, out of about 3 billion in the human genome.

You do know that the vast majority of those do nothing while the vast majority of the balance are deleterious don't you?

That's about a 7/1,000,000 chance that each person will be born with a mutation in the HAR1 gene.

I wonder what you would consider the odds of their being a benefical effect from a gene involved in brain delvelopment.

If we consider a population of 100,000 early hominids, then one needs only wait 1-2 generations before one of them has a mutation in the HAR1 gene. So we wait, oh, 10-20 generations until one of those mutations is beneficial. If that gene is subject to strong enough selective pressure, that gene will spread rather quickly throughout the population. Not all of the mutations need be sequential, either: beneficial mutation A could combine with beneficial mutation B through breeding rather than one organism starting with mutation A later obtaining mutation B.

The mutations are either sequencial (one at a time) or they all were fixed at the same time. Whenever a nucleotide is substituted the new codon must translate into a usefull amino acid.

In the 20 million years or so since we split off from Chimpanzees, there has been far more than enough time for the merely 18 separate mutations to have occurred. We're talking about something like 1,000,000 generations here! It's not hard to believe at all, to me, that such a change could occur within a few thousand generations.

That is wrong, the expansion of the human brain began between 2.5 mya and 1.5 mya. The split between the chimpanzee and human lineages (Homo) was around 5 mya.

http://www.mnh.si.edu/anthro/humanorigins/ha/a_tree.html

The estimates range from 5-7 mya for the actual split with 10 mya of total evolution. Your statistical scenerio is meaningless without referance to something tangible. Statistical probablity has to take into account deleterious effects. Your's did not even factor in the most common effects of mutations. You didn't calculate the odds of a single nucleotide being substituted becoming a meaningfull amino acid. Why don't you sharpen you pencil and rework your probablity statistics.

 

[mark kennedy]

We are talking past each other on literally every debate point. You already think you know more about the topic than the experts, and you are consistently inferring conclusions from the articles that are simply not supported.

I am not inferring anything, I am pointing out that this research represents an unprecedented overhaul of a highly conserved gene.

I think at this point you're just contradicting whatever I say, so I'll defer to whomever else wants to engage.

All I have really done is correct your misuse of terms like natural selection, evolution and mutation. If you want to drop out of the discussion that is your choice. It wont be long before I start a thread on the accelerated evolution of human specific genes. I trust you will be better prepared for the exchange if you decide to participate.

Match set!

 

[rmwilliamsll]

The mutations are either sequencial (one at a time) or they all were fixed at the same time. Whenever a nucleotide is substituted the new codon must translate into a usefull amino acid.


1. there is a distinction between mutation time and fixation time.
mutations happen all the time.
most are neutral, most never get passed to an offspring, of those that do, most are not fixed in the population. fixed meaning to have a relatively permanent place in the various alleles in a population at that loci or gene.

2. mutations that are spread out in a segment of dna (as in the example under discussion) probably happened one at a time, however sequential is not the right word. it is possible for one mutation in the male parent line say in position 3 and one mutation in the female line say position 5 to both appear in the offspring. extremely rare---yes but theoretically possible.

3. since most mutations are neutral a mutation that does change the codon to another amino acid in the protein only has to be passed on, deleterious mutations do get fixed in populations.

4. the other problem with this analysis is that the mutations may very have happened on a duplicated gene, if the original gene continued to function properly, all selection pressure is relaxed on the now pseudogene. then when the gene produced a useful protein product it came back under selection pressure.

 

[Chalnoth]

You do know that the vast majority of those do nothing while the vast majority of the balance are deleterious don't you?

And this precise effect explains why the gene has remained almost completely unchanged for so long, until a large selection pressure in favor of change in that gene occurred.

The estimates range from 5-7 mya for the actual split with 10 mya of total evolution. Your statistical scenerio is meaningless without referance to something tangible. Statistical probablity has to take into account deleterious effects. Your's did not even factor in the most common effects of mutations. You didn't calculate the odds of a single nucleotide being substituted becoming a meaningfull amino acid. Why don't you sharpen you pencil and rework your probablity statistics.

But the scenario where the mutation results in a meaningless amino acid only make it easier to produce a beneficial mutation! If the mutation is that destructive to the coding, the fetus would be unlikely to survive at all, and the parents would be able to try again much more quickly.

Unfortunately, I don't think anybody knows the exact probabilities of each kind of mutation. I mean, you have four possibilities:
1. A destructive mutation (fetus does not survive, either for very long in the womb, or for very long after).
2. A mutation that has no effect (won't spread through the population as a whole).
3. A mutation that degrades the survivability or reproductive capability of the organism (certainly won't spread through the population).
4. A mutation that increases the survivability or reproductive capability of the organism (will spread relatively quickly).

Unfortunately, of the ~400 possible insertion/change mutations in the gene, I don't think we have any way of knowing how many fit into each category. But we could just take the worst-case scenario, and state that only those 18 mutations which separate us from our ape brethren are beneficial to brain development (highly, highly unlikely, but why not, for the purpose of argument?).

Now, still with the assumption of ~100,000 hominid population, we know that any mutation in the HAR1 gene will happen about once every generation. But the probability for this mutation to be beneficial is about ~1/20. So it takes 20 generations for a beneficial mutation to occur. But there's still a relatively high mortality rate among humans, so even though we have rather high selection pressure in favor of well-developed brains, there's still a significant chance the hominid child in question won't ever grow up. So let's say it takes, on average, fifty tries for that gene to survive until it can actually spread.

So that's one mutation every 1000 generations that spreads throughout the population. Once the mutation has occurred, as long as the selection pressure is there, it will spread throughout the entire population. So we have 18 of these mutations to perform, or 18000 generations. Let's bump it up to a good round 20000 generations.

If every generation is 20 years, we have a mere 400,000 years required for the HAR1 gene to change all 18 base pairs.

So, combining a near worst-case scenario for the probability of a mutation being beneficial, and adding in a 1/50 chance that that mutation will spread throughout the genome, we still have a miniscule time scale, in evolutionary terms, for the full gamut of changes in the HAR1 gene to have occurred.

 

[mark kennedy]

The mutations are either sequencial (one at a time) or they all were fixed at the same time. Whenever a nucleotide is substituted the new codon must translate into a usefull amino acid.


1. there is a distinction between mutation time and fixation time.
mutations happen all the time.
most are neutral, most never get passed to an offspring, of those that do, most are not fixed in the population. fixed meaning to have a relatively permanent place in the various alleles in a population at that loci or gene.

You have left out the most important distinction of all, they have to translate into a usefull amino acid sequence. Then, and only then, does a mutation provide a selective advantage at a specific loci. I understand the basics of how a mutation become fixed but you are talking about accelerated evolution of a specific gene whether you realize it or not.

2. mutations that are spread out in a segment of dna (as in the example under discussion) probably happened one at a time, however sequential is not the right word. it is possible for one mutation in the male parent line say in position 3 and one mutation in the female line say position 5 to both appear in the offspring. extremely rare---yes but theoretically possible.

I would be interested in hearing the theory that postulates the probablity of such a conserved gene undergoing such a dramatic change in seqeunce. I don't have a lot of patience for generalities when we are talking about such a specific sequence. A nucleotide at a time not only seems unlikely it seems like fantasy. I don't know exactly what the amino acid sequence is but we are talking about 6 amino acids. A nucleotide at a time is an absurd probablity that is virtually incalcuable.

3. since most mutations are neutral a mutation that does change the codon to another amino acid in the protein only has to be passed on, deleterious mutations do get fixed in populations.

Yes, deleterious mutations do become fixed, far more the advantageous ones. That is why this one is far beyond the range of directly observed changes because they simply don't happen.

4. the other problem with this analysis is that the mutations may very have happened on a duplicated gene, if the original gene continued to function properly, all selection pressure is relaxed on the now pseudogene. then when the gene produced a useful protein product it came back under selection pressure.

Gene duplication would leave some trace and this one is highly conserved for 310 million years. There is very little doubt in my mind that a change in the amino acid sequence is not only unlikely it is impossible. There has to be a cause for this dramatic transmutation and a single nucleotide at a time is absurd in the extreme.

 

[rmwilliamsll]

A nucleotide at a time not only seems unlikely it seems like fantasy.


i posted these headlines from: http://www.pseudogene.org/human/index.php
awhile back

Comprehensive Survey of Processed Pseudogenes in the Human Genome

We have identified ~8000 processed pseudogenes plus ~4000 duplicated pseudogenes in the latest GoldenPath human draft genome.

Analysis of Chromosome 22 Pseudogenes and Transcription

By integrating several sources of pseudogene annotation, we have identified 525 pseudogenes or pseudogene fragments on chromosome 22 of the human genome NCBI Build34. Using data from tiling microarrays and EST sequences, we found that about 5% of them were potentially transcribed.

Analysis of Human Cytochrome c (cyc) Pseudogenes

We have identified over 49 cytochrome c (cyc) pseudogenes in the August 2001 freeze of the human genome draft.

gene duplication is a fact, a big fact, lots of pseduogenes where there is no selective pressure and they are free to make proteins or not. a pseudogene can easily manage to accumulate 18 single point mutations before it becomes useful or even transcribed.

 

[Chalnoth]

gene duplication is a fact, a big fact, lots of pseduogenes where there is no selective pressure and they are free to make proteins or not. a pseudogene can easily manage to accumulate 18 single point mutations before it becomes useful or even transcribed.

I really doubt that's going to happen very often, though. The probabilities of the final gene become pretty extreme if you ask the gene to mutate freely and randomly for a time, then suddenly become useful.

This sort of thing may be a good explanation for mutations that happened on a time scale of tens or hundreds of millions of years, such as the evolution of homeobox genes, but I doubt it could explain the mutations of the HAR1 gene. The mutation of this gene, when compared with the timescale involved, can really only be explained by relatively gradual mutations.

And Mark, you can't really possibly say that the mutation of the HAR1 gene couldn't possibly have been gradual unless you examine the result of each particular mutation (something that is quite hard to do, unfortunately).