More on the origination of new protein-coding genes

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Recently, we learned of an instance of the de novo origination of a new protein-coding gene in yeasts. This instance involved a mechanism or pathway that seems difficult to some, namely the random appearance of an open reading frame in an otherwise noncoding segment of DNA via judicious appearance of translation start and stop codons. The question naturally arises as to the relevance of such a pathway to real-life biology; was/is this a rather rare event that doesn’t really contribute to protein evolution, or is it a common means by which the protein-coding capacity of a genome is augmented?

A paper that is in press in Genome Research (Zhou et al., “On the origin of new genes in Drosophila”) gives us some insight into this question. The abstract of this paper summarizes things as well as I can:

Several mechanisms have been proposed to account for the origination of new genes. Despite extensive case studies, the general principles governing this fundamental process are still unclear at the whole genome level. Here we unveil genome-wide patterns for the mutational mechanisms leading to new genes, and their subsequent lineage-specific evolution at different time nodes in the D. melanogaster species subgroup. We find that, 1) tandem gene duplication has generated about 80% of the nascent duplicates that are limited to single species (D. melanogaster or D. yakuba); 2) the most abundant new genes shared by multiple species (44.1%) are dispersed duplicates, and are more likely to be retained and be functional; 3) de novo gene origination from non-coding sequences plays an unexpectedly important role during the origin of new genes, and is responsible for 11.9% of the new genes; 4) retroposition is also an important mechanism, and had generated approximately 10% new genes; 5) about 30% of the new genes in the D. melanogaster species complex recruited various genomic sequences and formed chimeric gene structures, suggesting structure innovation as an important way to help fixation of new genes; and 6) the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup. Finally, we survey gene frequencies among 19 strains from all over the world for D. melanogaster-specific new genes, and reveal that 44.4% of them show copy number polymorphisms within population. In conclusion, we provide a panoramic picture for origin of new genes in Drosophila species.

To be brief, I’d point out two things:

  • First, with regard to the earlier essay, the mechanism for gene origination described by Cai et al. would seem to be a significant contributor to new genes in the course of evolution (being responsible for almost 12% of the new genes identified by Zhou et al.). This answers the question I pose above – this mechanism is not impossibly rare, but a significant way by which new genes arise.
  • Second, almost 1/3 of the new genes identified by Zhou et al. are chimeras that involve the cobbling together of different sequences much as occurred with the origination of T-urf13. This brings into greater prominence this latter example of de novo origination of new genes.

There is much more to Zhou et al. than these points, and I would encourage readers to read the paper (in preprint form, as I have done, or in a more final form once it is processed by Genome Research). This is the best way to appreciate that this one pillar of ID thought, that new protein-coding genes cannot arise by “natural” means, is an illusion.

(This essay may also be found here.)

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If you happen to go to New-Mexico don’t miss the exhibition at the Hairy Museum of natural history. Some great pictures and a lot of information can be found in the beautiful article of Matt Celeskey. I’ve rarely seen so many fossils in... Read More

45 Comments

Very interesting research. Funny that when more research is performed many questions are answered and more questions arise. That’s the cool part of scientific research. Now compare this to Intelligent Design. Ask yourself, what does ID have to contribute to science?

Several million dollars?

Very interesting research!

But one thing puzzles me:

…the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup…”

Only 5 to 11 genes per million years? In a species with such a short generation time?

IIRC, humans and chimps differ in several hundreds genes (or, if you prefer, humans and the common ancestor of humans and chimps differ in half that many - still some hundreds). If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?

What am I missing here?

Only 5 to 11 genes per million years? In a species with such a short generation time?

IIRC, humans and chimps differ in several hundreds genes (or, if you prefer, humans and the common ancestor of humans and chimps differ in half that many - still some hundreds). If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?

Don’t forget that gene insertions and deletions can also be responsible for the differences.

Dave Wisker said:

Don’t forget that gene insertions and deletions can also be responsible for the differences.

I’m aware of these, but I don’t see how that can help much. I was talking specifically about the number of new genes, not merely about “differences”.

Let’s use specific numbers. From an older post here on PT (“Haldane’s non-dilemma”, by Ian Musgrave):

Recent comparisons of Human and Chimp genomes, using the Macaque as an out group, have given us a good idea of how many genes have been fixed since the last common ancestor of chimps and humans.

154

Actually, that’s 154 of 13,888 genes. Given that we have around 22,000 genes [3] in our genome, then if the same percentage of beneficial mutations holds for the rest of the genome, no more than 238 fixed beneficial mutations is what separates us from the last common ancestor of chimps and humans.

238 genes have been fixed! Now I’m not a biologist, so perhaps “238 genes have been fixed” does not imply that “238 new genes have appeared.” Is this were I’m going wrong?

If not, I don’t see how you can solve the discrepancy. Even if we assumed the same rate given for fruit flies also for humans (and I think that would be ridiculous if one compares the generation times and the generation size), we would get at most 66 new genes since the last common ancestor!

Björn said:

If not, I don’t see how you can solve the discrepancy. Even if we assumed the same rate given for fruit flies also for humans (and I think that would be ridiculous if one compares the generation times and the generation size), we would get at most 66 new genes since the last common ancestor!

238 “genes being fixed” most likely refers to the fixation of allelic gene forms, not the creation of new protein products. Additionally, I would not expect the rate of gene creation in drosophila to be representative of all species. If the rate of mutations arising is a limiting factor to the speed of evolution then you are right that we would expect drosophila to evolve faster. But if ecological or some other type of environmental or morphological constraint limits the rate of evolution, then all bets are off. For instance, perhaps the endemic retrovirus infection in primates speed new gene creation.

wikipedia nylon eating bacteria:

Scientists were able to induce another species of bacteria, Pseudomonas aeruginosa, to evolve the capability to break down the same nylon byproducts in a laboratory by forcing them to live in an environment with no other source of nutrients. The P. aeruginosa strain did not seem to use the same enzymes that had been utilized by the original Flavobacterium strain.[2] Other scientists were able to get the ability to generate the enzymes to transfer from the Flavobacterium strain to a strain of E.Coli bacteria via a plasmid transfer.[3] Genetic analysis of the plasmid led some scientists to the conclusion that the genes to produce one of the enzymes had most likely resulted from the combination of a gene duplication event with a frame shift mutation.[4] Further analysis has led to speculation that the fact that the frame shift was able to produce a functioning enzyme was related to the absence of stop codons in the duplicate gene.[5] Research has continued in the hope of better understanding the mechanisms involved in the evolution of new enzymes, and because of the possible value of bacteria that can metabolize man made molecules to toxic waste cleanup.

A few more examples of de novo evolution of new genes.

Nylon eating bacteria of course. Which happened in real time. A frameshift within an existing gene created a new enzyme activity capable of eating a novel substrate, nylon.

The T cytoplasmic sterility trait in corn, which was explained at length by Arthur Hunt, the current poster here on PT a while back.

We know that evolution can create new information because we see it happen. So much for the creos.

Bjorn says: “Only 5 to 11 genes per million years? In a species with such a short generation time?” IIRC, humans and chimps differ in several hundreds genes … If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?”

And asks: “What am I missing here?”

.

Obviously an as of yet undiscovered mechanism(s), and the edge of evolution via RM+NS.

bigbang said:

Obviously an as of yet undiscovered mechanism(s), and the edge of evolution via RM+NS.

Nobody asked for your uninformed opinion. I prefer scientific explanations, based on evidence. So shut up, please.

Larry writes:

238 “genes being fixed” most likely refers to the fixation of allelic gene forms, not the creation of new protein products

Exactly right.

As I don’t have access to the paper I’m afraid the always interesting panoramic view seems a bit clouded to me. Let me see if I got this right; in one species we can see that new genes arise by three major mechanisms, duplication (~ 40 %), chimerism (~ 30 %), and de novo (~ 10 %)?

In any case I’m impressed by the prevalence of chimerism. But then again evolution proves itself again and again to be the ultimate tinkerer.

Björn said:

238 genes have been fixed! Now I’m not a biologist, so perhaps “238 genes have been fixed” does not imply that “238 new genes have appeared.” Is this were I’m going wrong?

Now I’m not a biologist either, but if we expose our confusions we can get help to sort them out.

So my layman picture is this; we have to look at variation and selection independently. As regards new genes I assume that in the same way that some alleles can be fixed by drift it can also happen to new genes. I.e. some new genes are beneficial or harmful and selection will fix them, other will be near neutral and drift will fix them. (In both cases quite possibly to extinction - albeit I don’t know if the technical term is “fixed” then.)

The post you referred to explicitly looked on how many genes that had been fixed by positive (I think) selection. That will AFAIU include all variation that is beneficial, beneficial new genes as well as old alleles that happen to become beneficial. Remaining fixation was mentioned above, neutral or negative.

This is probably ridiculously simplified. For example, I hear that genes near selected genes may be driven along to fixation by selective sweeps. Paleoanthropologist John Hawks et al have papers claiming that human evolution rate has increased in historical times two order of magnitudes. Most of those genes are swept along AFAIU.

The mechanism they identify is selection (mostly on already existing variation). They propose the increased rate is due to changes in environment (reason for selection) and increased population (response to selection). If you look at the last figure, over selected variants (here fixed and near fixed variants), they predict ~ 3 selected variants/generation. Quite higher rate than ~ 10 new genes/10^6 years.

[If I take this rate and revert to their proposed baseline rate, and use the proposed differences of order 1000 fixed alleles (YMMV) between humans and chimps, I get the last possible human-chimp split from an ancestor at roughly 10^6 years. So maybe their data is reasonable, at least in that regard.]

So while you have trouble reconcile the post with hominid evolution, I don’t. So where did I go wrong, I wonder? Pointers appreciated.

Bigbang is providing us with some excellent first hand evidence of why ID Creationism is scientifically vacuous.

Björn said:

bigbang said:

Obviously an as of yet undiscovered mechanism(s), and the edge of evolution via RM+NS.

Nobody asked for your uninformed opinion. I prefer scientific explanations, based on evidence. So shut up, please.

Please don’t forget that bigbangBigot also serves as an excellent first hand example of the extraordinarily pernicious effects Intelligent Design Creationism has on a person’s intellectual health and ability to distinguish facts from falsehoods.

PvM said:

Bigbang is providing us with some excellent first hand evidence of why ID Creationism is scientifically vacuous.

As someone who toyed with YECism, I have first handed experienced the disastrous effects on faith and science because of a foolish position. Insisting, against all evidence, and without clear theological requirements, that the earth is young causes much harm. That’s one of the reasons why people with higher IQ and more advanced educations tend to be less religious. After all, finding out the truth about science and religion can be quite a shock to faith. It’s somewhat ironic that YEC and ID Creationism are contributing strongly to the decrease in religious faith, far more than any atheistic concept ever could.

Stanton said:

Please don’t forget that bigbangBigot also serves as an excellent first hand example of the extraordinarily pernicious effects Intelligent Design Creationism has on a person’s intellectual health and ability to distinguish facts from falsehoods.

PvM said:

Bigbang is providing us with some excellent first hand evidence of why ID Creationism is scientifically vacuous.

It’s like this one ghost in The Real Ghostbusters cartoon once said, “When you become obsessed with the enemy, you become the enemy.”

PvM said:

It’s somewhat ironic that YEC and ID Creationism are contributing strongly to the decrease in religious faith, far more than any atheistic concept ever could.

PvM said:

It’s somewhat ironic that YEC and ID Creationism are contributing strongly to the decrease in religious faith, far more than any atheistic concept ever could.

Well, if they’re going to insist that their religion contradicts the evidence based conclusions of scientists (biologists, but also other fields), anybody who believes them would have to pick… one or the other. Notice that those that then pick religion would have been religious anyway, so this approach can’t bring people to religion, it can only drive them away from it.

Henry

Björn said:

Very interesting research!

But one thing puzzles me:

…the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup…”

Only 5 to 11 genes per million years? In a species with such a short generation time?

IIRC, humans and chimps differ in several hundreds genes (or, if you prefer, humans and the common ancestor of humans and chimps differ in half that many - still some hundreds). If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?

What am I missing here?

And in Haldanes non Dilemma” I wrote:

Recent comparisons of Human and Chimp genomes, using the Macaque as an out group, have given us a good idea of how many genes have been fixed since the last common ancestor of chimps and humans.

154

Actually, that’s 154 of 13,888 genes. Given that we have around 22,000 genes [3] in our genome, then if the same percentage of beneficial mutations holds for the rest of the genome, no more than 238 fixed beneficial mutations is what separates us from the last common ancestor of chimps and humans.

The difference is that these 238 genes are allelic variants of existing genes (ie beneficial mutations of existing genes), not the De novo genes reported in this paper (completely new genes from duplication/fusion of existing genes or non-coding DNA becoming coding). As far as we know, there are no De novo genes in humans compared with chimpanzees. The total number of gene fixations in Drosophillia (including De novo genes and allelic substitutions) is on the order of a 1000 or so over a similar time frame (I don’t have the exact figures to hand at the moment).

Ian Musgrave said: As far as we know, there are no De novo genes in humans compared with chimpanzees.

Wow. That’s something cool I didn’t know this morning. Now what did ID predict in this situation ?

Science is so much more exciting than GodDidIt.

Stanton said:

It’s like this one ghost in The Real Ghostbusters cartoon once said, “When you become obsessed with the enemy, you become the enemy.”

When it comes to Darwin-bashers, I can’t help but cite Eduardo: “We’re like scienteests, man.”

White Rabbit (Greg Goebel) http://www.vectorsite.net/tadarwin.html

6) the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup.

At this rate it would take 90909090909.09090909090909 years for the evolution of one million new genes! This is certainly more than the 3427257351.98773635 years evolutionists say life has been evolving. There are probably about a million genes difference between PZ Myers and my hound dog!

Evolutionists still hold on to their religion no matter how adsurd it seems even to its own high priests. Why can’t they just read the Bible?

Bubba Von Grubba said:

6) the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup.

At this rate it would take 90909090909.09090909090909 years for the evolution of one million new genes!

So far so good. Except there are drastically fewer genes in even the most complex organism.

This is certainly more than the 3427257351.98773635 years evolutionists say life has been evolving.

Who has said that? Ever?

There are probably about a million genes difference between PZ Myers and my hound dog!

Unsubstantiated. Evidence please.

Evolutionists still hold on to their religion no matter how adsurd it seems even to its own high priests. Why can’t they just read the Bible?

Please someone tell me this is a Poe.

Torbjörn Larsson, OM said: … I get the last possible human-chimp split from an ancestor at roughly 10^6 years.

For what it may be worth:

In “The Monkey Puzzle” (1982)and again in “The First Chimpanzee” (2001), John Gribbin and Jeremy Cherfas argue for a LCA of chimp and man of about 4 million years.

In http://web.uccs.edu/fcoolidg/Hodgso[…]comments.pdf we find “the human/ chimpanzee split seven million years or so ago.”

I believe I have seen other figures too in the 7 to 4 range.

Concerning the Bjorn’s question concerning rate of evolution,

bigbang opined:

Obviously an as of yet undiscovered mechanism(s), and the edge of evolution via RM+NS.

whereas

Ian Musgrave replied:

The difference is that these 238 genes are allelic variants of existing genes (ie beneficial mutations of existing genes), not the De novo genes reported in this paper (completely new genes from duplication/fusion of existing genes or non-coding DNA becoming coding). As far as we know, there are no De novo genes in humans compared with chimpanzees.

Yet again, what is “obvious” to bigbang turns out to be false.

Bubba Von Grubba said:

6) the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup.

At this rate it would take 90909090909.09090909090909 years for the evolution of one million new genes! This is certainly more than the 3427257351.98773635 years evolutionists say life has been evolving. There are probably about a million genes difference between PZ Myers and my hound dog!

Evolutionists still hold on to their religion no matter how adsurd it seems even to its own high priests. Why can’t they just read the Bible?

(ignoring Poe’s Law for the sake of argument) Yet according to data presented by Ian Musgrave, there are only 22,000 total genes in the human genome. Therefore, if we plug in the rate for D. melangaster, it would only take 2 billion years - well within the time span indicated.

Of course, it is problematic to assume that the rate is constant for all species for the entire course of evolution, but it does show that the conclusions fall in line with confirmed data.

Perhaps in no discussion I have seen have the creationists so completely and clearly revealed a complete lack of understanding of the science involved. They completely confound the de novo gene origins (which is quite rare), from the evolution of new functions in old genes. As well as generic rates of sequence change most of which are functionally neutral.

On an actual science note I did not find the rate for chimerism operating as a mechanism to be particularly surprising. It generally seems to be a handy mechanism for the rapid evolution of new protein regulation, and is consistent with thinking about proteins as functional domains.

Someone can probably clarify for me some confusion along the lines of Björn’s question.

If the same genes produce distinctly different species by turning on and off at different times during development, or interacting in new ways, is this regarded as an allele change? Is it easy to track down which genes have had their timing altered, and how?

Is it possible some constellation of alleles that enable rational thinking got turned off in creationists sometime in infancy? Is it possible that early indoctrination can physically alter gene expression? This might explain a lot.

Bubba Von Grubba said:

There are probably about a million genes difference between PZ Myers and my hound dog!

In the words of Storngbad:Absolutely not the case.

In lieu of a direct response, here is an entertaining pastiche: It is impossible that the US treasure prints all the money in circulation. The US GDP is probably about 412,231,122,322,123.1231211 dollars, and A single printing press at the US treasury might print 1,123.99 bills a minute. At that rate it would take 697,787.15 years to print the money Americans spend every day! Therefor, some mechanism other than the printing press must be responsible for creating paper money.

There are at least 5 major problems with this argument, can you find them all?

Flint said:

Someone can probably clarify for me some confusion along the lines of Björn’s question.

If the same genes produce distinctly different species by turning on and off at different times during development, or interacting in new ways, is this regarded as an allele change? Is it easy to track down which genes have had their timing altered, and how?

Is it possible some constellation of alleles that enable rational thinking got turned off in creationists sometime in infancy? Is it possible that early indoctrination can physically alter gene expression? This might explain a lot.

These questions are … awesome. 10 points.

In my opinion you would call different forms of regulatory regions alleles. Wikipedia alleges this usage is not idiosyncratic. [http://en.wikipedia.org/wiki/Allele]

The term allele should only be applied to particular base pair sequences and not the behavior of a gene. If an allele produces different effects in different genetic backgrounds this is called epistasis, [http://en.wikipedia.org/wiki/Epistasis] and the different effects are not attributed to different alleles.

Tracking differences in gene expression is not precisely easy, but several standard laboratory practice allow for remarkable detailed studies. You can use PCR or qRT-PCR to look for the unique mRNA produced by the genes of interest. This involves destructive tissue sampling, but can reveal a detailed assay of the genes expressed in a tissue. Particularly fun are studies of viral gene expression, since a detailed time analysis of the expression of every viral gene can be done. Alternatively several methods of florescent labeling can be used. Genetically linked co-expression of a florescent marker with a gene of interest or antibody florescent labeling techniques can produce a visuals map of gene expression across the body of an organisms. This gene expression map can be directly examined by use of a microscope. This can be particularly revealing for genes which control development and hence have interesting spatial patterns of activation such as HOX genes.

In regards to your most excellent concluding question I would actually have to answer in the affirmative. While there is no particular evidence of a cohort of ‘rational genes’ existing, environmental factors can create heritable differences in genes expression without altering the genetic code. [http://en.wikipedia.org/wiki/Epigenetics] Epigenetic changes can be induced by a large number of factors many of which may represent adaptive responses. As such nutrition, hormonal state or any cue which could foreshadow the future environment of offspring could at least in theory affect a persons mental development through epigenetics.

Flint said:

If the same genes produce distinctly different species by turning on and off at different times during development, or interacting in new ways, is this regarded as an allele change?

I’m taking a second stab at answering this, since my first answer seems to brief and confused. Many morphological differences between species or individuals can be attributed to different patterns of gene expression, as you say. Patterns of gene expression, however, are controlled by non-coding regulatory regions and the complex interaction of regulatory genes. Generally allele is only used to refer to different gene-forms within a single species. But, it is sensible to say that a the pattern of gene A’s expression is different between species A and B because A and B have different regulatory alleles, though this may be a significantly non-standard usage of the word. The same gene in two different species is generally referred to as homologous forms. So it would be more standard to attribute the difference in the gene expression pattern to fixed differences in homologous regions of DNA.

It sometimes occurs that one allele in species A is more closely related to an allele in species B than it is two the alternative allele in species A. (I think I got this from Gould’s big book, but I not positive.)

Ian Musgrave said:

The difference is that these 238 genes are allelic variants of existing genes (ie beneficial mutations of existing genes), not the De novo genes reported in this paper (completely new genes from duplication/fusion of existing genes or non-coding DNA becoming coding).

Thanks for the definite answer.

As far as we know, there are no De novo genes in humans compared with chimpanzees.

Now that’s really amazing! All the differences (bipedal walking, larger brain, ability to speak etc.) all are only due allelic variants, not to new genes?!

Björn said:

As far as we know, there are no De novo genes in humans compared with chimpanzees.

Now that’s really amazing! All the differences (bipedal walking, larger brain, ability to speak etc.) all are only due allelic variants, not to new genes?!

Some of the differences are also due to post-translational and epigenetic factors, in that different exons and introns in certain genes are conserved and excised (respectively).

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Some of the differences are also due to post-translational and epigenetic factors, in that different exons and introns in certain genes are conserved and excised (respectively).

(syntax error repost.)

Exon/intron magic happens post-transcription, pre-translation. Or are you actually referring to the post-translational modification of a protein product?

Larry Boy said:

Stanton said:

Björn said:

Some of the differences are also due to post-translational and epigenetic factors, in that different exons and introns in certain genes are conserved and excised (respectively).

Exon and intron magic happens post-transcription, pre-translation. Or are you in fact referring to post-translational modifications of the protein product?

Yes: you’re right (sorry, it’s too early in the morning for me) : and yes, many of the major differences between chimpanzee and human concern post-transcription/pre-translational differences of the gene products, as well as different post-translational modifications of the gene products, as well.

As far as we know, there are no De novo genes in humans compared with chimpanzees.

To clarify this important point further…

All genes come from some ancestor DNA sequence.

If a gene arises because a non-coding sequence gains start and stop codons, or because partial elements of other genes combine at a new locus, that’s pretty much a straightforward “de novo” gene.

If a gene arises because of gene duplication, it may be called a de novo gene when it gains enough difference from the ancestor gene, or it may simply be referred to as a “copy” of the ancestor gene, especially if it is unexpressed. If a protein with novel function eventually results, almost anyone would call the duplicate a novel gene by that point.

When some copies of a gene pick up mutations, but the locus of the gene on the chromosome doesn’t change, then the novel sequence is usually thought of as an allele of the original gene, at least within the same species. Most of the genetic differences between humans and chimpanzees are more or less allelic differences, relative to common genes that were also present in the most recent common ancestor. Different versions of the same gene, so to speak.

My ol’ houn’dog has a million genetic differences compared to that pesky PeeZee Myers

Or whatever it was that parody poster Bubba said.

Actually, this could be true or nonsensical, depending on what you mean by “genetic differences”.

If you mean base pair differences between the actual sequence of human genes versus the same genes in canine species, it may be true. It may even be an underestimate.

If you mean actual entire genes possessed by one species but not the other, it can’t possibly be true, because humans are currently believed to have only tens of thousands of discrete genes, as we currently define them. And humans and canines share somewhat recent common ancestry.

I apologize for any over simplifications,as I have not been able to read any of the publications associated with this, and am going off only a talk delivered by Olivier Fedrigo at the Evolution 2008 conference. The group in question examined genome scale changes in primates primarily chimps and humans. In general with the exception of the gene FOXP2 there was little evidence of positive selection in the protein coding sequences of genes associated with neurological development. What was interesting is that focusing purely on regulatory elements they did find evidence suggestive of a lot of positive selection for those genes when comparing human and chimps. Now as a genome wide study there are a variety of issues with firm conclusions of cause and effect, but the data does support the developing story coming out of the evo-devo world that implicates the evolution of new species to changes most frequently in developmental regulation.

harold said:

And humans and canines share somewhat recent common ancestry.

A common ancestor from about 80 to 70 million years?

Dan said:

Concerning the Bjorn’s question concerning rate of evolution,

bigbang opined:

Obviously an as of yet undiscovered mechanism(s), and the edge of evolution via RM+NS.

whereas

Ian Musgrave replied:

The difference is that these 238 genes are allelic variants of existing genes (ie beneficial mutations of existing genes), not the De novo genes reported in this paper (completely new genes from duplication/fusion of existing genes or non-coding DNA becoming coding). As far as we know, there are no De novo genes in humans compared with chimpanzees.

Yet again, what is “obvious” to bigbang turns out to be false.

But of course, he’ll keep repeating the same lies until the end of time, no matter how many times he’s shown to be wrong.

All he knows how to do is beat dead horses, and no matter how obvious it is, he’ll never see that they’re dead. Knowing the truth might impair his ability to lie, and we can’t have that, now can we?

Björn said:

238 genes have been fixed! Now I’m not a biologist, so perhaps “238 genes have been fixed” does not imply that “238 new genes have appeared.” Is this were I’m going wrong?

Yup, as others, I think have pointed out, that is where you went wrong. As was pointed our earlier this is the number of fixed allelic variations and not the number of new genes

Stanton said:

Björn said:

As far as we know, there are no De novo genes in humans compared with chimpanzees.

Now that’s really amazing! All the differences (bipedal walking, larger brain, ability to speak etc.) all are only due allelic variants, not to new genes?!

Some of the differences are also due to post-translational and epigenetic factors, in that different exons and introns in certain genes are conserved and excised (respectively).

Not to mention differences in gene expression, especially during development. That seems to be a very importanr mechanism in evolution and may play one of the largest roles in the differences between chimps and humans.

A common ancestor from about 80 to 70 million years?

I meant recent in terms of evolution, of course.

That’s extremely recent compared to what would be expected if you chose a species at random from the biosphere to compare to humans.

I mean seriously, just the fact that we’re both placental mammals…

This reference says 95 million years, which is still “fairly recent” in the way I meant it.

http://www.mrcfgu.ox.ac.uk/research[…]y/Webber2005

Flint said:

If the same genes produce distinctly different species by turning on and off at different times during development, or interacting in new ways, is this regarded as an allele change? Is it easy to track down which genes have had their timing altered, and how?

Is it possible some constellation of alleles that enable rational thinking got turned off in creationists sometime in infancy? Is it possible that early indoctrination can physically alter gene expression? This might explain a lot.

Larry Boy has already responded to some of this, but I wanted to add my two cents worth: the twin studies at the University of Minnesota have found convincing evidence that “religiosity” is at least partly genetically determined (don’t have handy references, but interested parties can search for the papers of Tom Bouchard and Matt McGue). And, because behavioral phenotypes are produced by the interaction of genotype and environment, religious persons tend to selectively breed with other religious persons, enhance those genetic tendencies by immersing themselves in religion-reinforcing environments, and have children with high religiosity indices that are raised in religious environments, thus perpetuating the phenotype. I view creationism as one point along the religiosity phenotype continuum. If an individual is a creationist because of their individual genetic (allelic) contributions, then they will always be a creationist. This likely describes some of my relatives. However, if an individual is a creationist because of a large environmental input, but minimal genotypic influence, their behavioral phenotype will be more plastic and they can escape from creationist thinking. My father is probably an example.

The fascinating question that has driven my own research (albeit on other behaviors) is, which genes are involved and how do the different alleles change the phenotype?

Vaughn

Vaughn Wrote:

And, because behavioral phenotypes are produced by the interaction of genotype and environment, religious persons tend to selectively breed with other religious persons, enhance those genetic tendencies by immersing themselves in religion-reinforcing environments, and have children with high religiosity indices that are raised in religious environments, thus perpetuating the phenotype.

Might these tendencies also be related to genetic tendencies toward needs for security and nurture that are more common in the young and adolescent stages of development?

In other words, some people don’t mature and adopt a more objective relationship with the real world; and authoritarian religion becomes a “surrogate parent” that these people attach themselves to. Their clustering together in such environments would be simply another manifestation of the fear and insecurity that accompanies aborted emotional development.

Another confounding factor could be mental illnesses such as schizophrenia and bipolar types of depression. For these people, the real world does not offer much in the way of coherence and consolation. Authoritarian religion may again be a surrogate.

Might these tendencies also be related to genetic tendencies toward needs for security and nurture that are more common in the young and adolescent stages of development?

This line of discussion started off with a joke. The religious beliefs a person adopts are environmentally determined to a massive degree.

But there is a trait that creationists have in spades, relative to others, and it may have a genetic component (or not, for all I know), and it isn’t “religiosity”, which is quite common in non-fundamentalists as well -

It’s authoritarianism.

They tend to be hyer-concrete thinkers who, first of all, identify ethical behavior as consisting entirely of obedience to literal and arbitrary rules, out of fear, and who second of all, want to set themselves up as the ones who decide which set of rules everyone else has to follow. And they fantasize of inflicting brutal punishments on those who don’t obey them. And they gravitate naturally toward political movements that deny human rights or common responsibilities.

That’s what it’s all about.

Björn said:

Very interesting research!

But one thing puzzles me:

…the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup…”

Only 5 to 11 genes per million years? In a species with such a short generation time?

IIRC, humans and chimps differ in several hundreds genes (or, if you prefer, humans and the common ancestor of humans and chimps differ in half that many - still some hundreds). If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?

What am I missing here?

you’d have to take into account the Earth is Billions of years old. Life is estimated to start at 3.6 billion years ago, http://nitro.biosci.arizona.edu/cou[…]origins.html … this gives plenty of time for the genes to add up.

Tylor said:

Björn said:

Very interesting research!

But one thing puzzles me:

…the rate of the origin of new functional genes is estimated to be 5 to 11 genes per million years in the D. melanogaster subgroup…”

Only 5 to 11 genes per million years? In a species with such a short generation time?

IIRC, humans and chimps differ in several hundreds genes (or, if you prefer, humans and the common ancestor of humans and chimps differ in half that many - still some hundreds). If the human-chimp split was only about 6 million years ago, how can we have acquired all these genes in that time?

What am I missing here?

you’d have to take into account the Earth is Billions of years old. Life is estimated to start at 3.6 billion years ago, http://nitro.biosci.arizona.edu/cou[…]origins.html … this gives plenty of time for the genes to add up.

apologies, i didn’t read your entire comment, it’s an interesting question worth researching.

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This page contains a single entry by Arthur Hunt published on June 24, 2008 11:33 PM.

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