A Simple Gene Origination Calculation

_{PaV
July 27, 2008

Intelligent Design

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Intelligent Design}

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In this month’s Nature Genetics, there is an article by Zhou, et. al., dealing with the generation of new genes in Drosophila melanogaster—the fruit fly. While only having access to the abstract, I nonetheless was struck by one of their findings: the rate of new functional gene generation. As finding number 6 in the abstract, the authors write: “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.”

Noting that Drosophila melanogaster has 14,000 genes (a very low gene number), the simply calculation is this: 14,000 genes/8 new functional genes per million years= 1.75 billiion years for the formation of the fly genome. This, of course, assumes that somehow the fly is ‘alive, and reproducing’ the entire 1.75 billion years—-this, without the aid of a full-blown genome. If we apply this to the monkey/human difference which, IIRC, is about a 1000 genes, then using this same rate, it would take 200 million years for man to have evolved from the monkey. This published rate for new functional gene generation cannot be good news for Darwinists.

Here’s the link to the abstract.

Comments

sparc: First of all, I really believe that my assumptions are right, and I invite you to tell where they should be wrong. In a sense, they are not assumptions at all, but very simple facts about probability. Regarding the immune system, the scenario is completely different. Primary antibody diversification is a process which uses random variation very intelligently targeted to generate a repertoire of basic antibody specificities to cover, at a low specificity level, a search space which is very big, but not immense, referring to possible epitopes in nature (an epitope is a very small aminoacid sequence, usually a few aminoacids, or up to ten -fifteen). Even so, the basic repertoire is very unspecific, and can ensure only a low level interaction with possible epitopes. Antibody maturation "after" primary response, instead, is a typical process which utilizes random variation very intelligently targeted plus very intelligent selection to increase the specificity of the immune response. Indeed, the process utilized here is the same as used in modern protein engineering: the results of targeted random variation are "measured" against the original epitope, and intelligent selection takes place (obviously, here selection includes very specific informatioon about the target, that is the epitope itself, and is therefore very efficient). So, as you can see, there is nothing in what we know about antibody generation which is inconsistent with my "assumptions". Antibody generation is a perfect example of intelligent engineering using the realistic resources of probability. It is therefore perfectly natural and reasonable that the immune system of birds or mammals can "produce antibodies against antigens that they or their ancestors never encountered before".gpuccio_{July 29, 2008
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Moderators: Re Mr King at 33 above. He has no permission to use my personal name in this blog or elsewhere. This is relevant first as there is a known asymmetry between ID supporters and opponents, given the issues raised in e.g. Expelled. Mr King either knows, or should know that. Secondly, in my case, I have found that use of my personal name and/or contact opens up to spam attacks. (I have retained in my personal site, ways to find my name and contact, but that is for responsible behaviour. What was done above is at minimum grossly irresponsible, and highly disrespectful.) I must therefore ask Mr King, on pain of further, more serious appeal to the Moderators, to cease and desist. GEM of TKIkairosfocus_{July 29, 2008
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gpuccio:
Those are named “de novo genes”. Nobody knows how they arise. They are certainly vastly beyond any probabilistic resource.
How can you establish a very low upper bound on the probability of an event when nobody knows its cause(s)?CEC09_{July 29, 2008
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The real fact is that it doesn’t matter. A search of 1:10^100, for all practical purposes, is as impossible as a search of 10^130, if we don’t incorporate information about the desired result in the search. And the only principle which can incorporate that kind of information is design.
If your assumptions were right it would be unlikely that your very own immune system would ever generate any functional antibody. BTW, you may read a little bit on immunoglobulin gene diversification in birds that heavily relies on pseudogenes and gene conversion. You will find out that birds and those mammals that employ the same mechanism to generate antibody diversity can indeed produce antibodies against antigens that they or their ancestors never encountered before.sparc_{July 29, 2008
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CEC09:
the rate of human evolution has accelerated by TWO orders of magnitude in recent times as a consequence of the population explosion and shifts in living conditions.
1, how recently has there been a significant shift in living conditions for human/humanoid species? 10,000 years? Even a 100 times increase in evolution means little with this much time accounting for it. The vast lions share of the 6 million years of interest is at the slower pace. What of the fruit fly, has its environment not been affected by modern farming practices. I'm sure they love fruit orchards. We also see that population (which until about 10,000 years ago was miniscule for the human lineage) benefits evolution. Fruit flies vastly outnumber us, don't they? They certainly vastly outnumbered our ancestors 1/2 million years ago. Every which way you turn, evolution should be happening vastly more slowly in humans than in fruit flies. My calculations suggest that, per generation, humans have evolved over 4 orders of magnitude faster than fruit flies. That, in light of the fact that there are many more fruit flies than humans (especially averaged out over the 6 million years.) # generations in 6 million years: Human 600,000. Fruit fly 600,000,000. # new genes during this time: Fruit fly: 50 (8 per mil * 6) Human: 689 # new genes in human during this time if they evolve at fruit fly's rate (per generation) 0.05 Difference in pace: about 14,000 to 1. dacook, "I none has been observed, how do we know it ever happens?" If one species of fruit fly has a gene that all other species don't have, a new gene must have come from somewhere. It does not require observing the new gene appearing to determine this. However, this observation does not give us the cause -- was the new gene the product of dumb luck or of an active agent.bFast_{July 29, 2008
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Paul Giem #27: "(Comment 49. Note: read carefully before replying, to avoid personal embarrassment.)" Thanks for the warning. That is such a kindness. You are a Christian in the best sense.Daniel King_{July 29, 2008
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I'd like to see the whole paper. Maybe someone who knows more about fruit fly research can tell me if any "new functional genes" have actually been observed to arise in all the generations of Drosophila studied? If even one has been observed, it seems that a rate could be calculated, rather than having to be estimated. I none has been observed, how do we know it ever happens?dacook_{July 29, 2008
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You did mean 1200 times more generations for fruit flies than for humans, I hope.
Thanks, Paul Giem. I was a bit rushed. Ten years is about 1200 times as long as 3 days.
Even in the best-case scenario, where the ancestor is genetically precisely between modern chimpanzees and modern humans, the genetic distance between modern humans and the ancestor would still be half of that between modern humans and modern chimpanzees.
I'm glad you brought this up. It's more reasonable, though somewhat simplistic, to think of chimps and humans as separated by 12 million years than by 6 million years.CEC09_{July 29, 2008
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bFast, extrapolation is regarded as highly dangerous throughout science, not to mention statistics. There are many examples of the errors it leads to. One of the reasons I introduced the Hawks et al. paper to the discussion is that it gives very strong evidence that the rate of human evolution has accelerated by TWO orders of magnitude in recent times as a consequence of the population explosion and shifts in living conditions. In other words, extrapolation of the human present to the human past, or vice versa, leads to grossly incorrect conclusions. When within-species extrapolation of the rate of genetic innovation is so strongly contraindicated for humans, and has been shown to be strongly related to population size, how can you possibly defend extrapolating results for a species group with populations that have long been much larger than the present human population to the human species? My objection to extrapolation of the numbers in the Zhou et al. abstract is not merely a matter of principle. Rigorous scientific study of the human genome clearly tells us not to extrapolate. This is not just one of my unexpert guesses.CEC09_{July 29, 2008
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CEC09:
you definitely cannot take rates and percentages from one species group and use them to make estimates for a species under quite different circumstances.
I fail to follow your reasoning here. While I would agree that you cannot use the rate of evolution of one species to determine the rate of evolution of another species down to multiple decimal places. However, we are discussing orders of magnitude here. We should be able to get some sense of orders of magnitude accross different genetic lines. This idea that we can know nothing from evidence extrapolation is just as silly as the idea that we can determine with precision via extrapolation. We need to get beyond this simple black and white thinking.bFast_{July 29, 2008
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CEC09: I read the abstract, and I really think that it is impossible to comment on it without reading the whole paper, which I can't. I will therefore make a few remarks about the above discussion, and especially about some of the many points you raised. You say (#4): "I still wonder exactly how de novo formation works". Nobody knows how it works. We just know that we find in species genes which have no significant homology with other known genes, even in a very general way. Those are named "de novo genes". Nobody knows how they arise. They are certainly vastly beyond any probabilistic resource. In essence, any kind of gene must have been, in the beginning, a "de novo" gene. Then, gene families are observed, where homologies can be found between the components of the same family. But nobody knows how "de novo" genes first arise, and in reality nobody knows how and why genes which have some homology are related. Even accepting some form of descent from one gene to the other, in most cases the mechanism of change is not known. The proposed mechanism of random variation and some form of selection is comnpletely impotent to generate those kinds of effects, as demonstrated by all the various calculations we have often discussed here at UD. You say: "And what is a non-functional gene? Does that mean it doesn’t yield a product, or does it mean that the product does not serve a function in the proteome?" Usually we call "gene", or more precisely "protein coding gene", those DNA sequences which have the characteristics of being transcribed and translated. That can be an inference from the structure of the DNA sequence, or we can have the evidence of the transcription and translation (in other words, we can know the mRNA or the protein). But the number of genes is often merely deducted by the analysis of the DNA sequence, and many studies about homologies are conducted in the same way. Obviously, when the protein is known, and so its function, the gene can be studied in a more realistic way. Pseudogenes are genes which are very similar to functioning genes, but are no more functional. I think that usually they are neither transcripted nor translated, but I would not take anything for granted in this very difficult subject: anything we actually know about non coding DNA (including pseudogenes) is in my opinion highly provisional. Finally, I am not sure, but I don't think we have evidence of translated proteins which have no function in the proteome, and which are there, waiting to be magically transformed by random mutations to acquire a purpose. Usually, a cell is a very crowded place, and each protein has its role. You say: "F2XL, is your problem here that the abstract says indirectly that there are in fact non-coding regions in the genome that don’t serve a function? After all, turning a functional non-gene region into a gene would stop that region from serving its prior function." I don't think the abstract says that. There was a thred some time ago about a much more specific work about the formation of a de novo gene (I don't remember the name of the thread or of the article), and the possibility was discussed that a de novo gene originared by mutations from a segment of non coding DNA. The interesting thing is that the supposed "progenitor" sequence seemed to be transcribed and functional. So, your question is legitimate, and indeed it is the same question which i made in that thread: if the original non coding DNA was transcribed and functional, what happens when it gives rise to a protein coding gene? (In the case discussed, there was no evidence of duplication of the original sequence). Moreover, the results of the ENCODE project seem to show that practically all the genome is transcribed. That does not prove that it is functional, but it is a good step in that direction. You say: "Didn’t Dr. Dembski argue in “Searching Large Spaces” and other writings that even one de novo functional gene is very unlikely to be discovered by random search?" Yes, he did, and it is. If we really find de novo genes in species, and we do find them, and will find them ever more, that is only a good reason to ask ourselves how those genes ever did arise. The only reasonable answer is design (see next point). You say: "Or did he say that base-pair sequences he specified as a target were very unlikely to be hit? The abstract seems to address formation of any new genes that do something, not just genes that do what the researchers had in mind before looking at the genome. Isn’t this a much bigger target than Dr. Dembski considered?" That's a very important and pertinent question, and often a cause of misunderstanding. The subject is vast, but I will just outline some aspects: a) Nobody really knows how big the target of functional proteins is, but we have all the reasons to think that it is very, very small compared with the immense search space of all possible protein sequences. Let's make an example, amd take the generic search space of all proteins of 100 aminoacids (which are indeed very small proteins). The whole search space is about 10^130. That's something! But how many of these proteins can be functional? Nobody really knows, but even if we take "functional" in a very big sense, that is "able to have some useful function in some kind of living being", still we have to remember that there are a lot of constraints, some known, some unknown, to that result: proteins have to be able to fold, and to fold in some ordered way, usually corresponding to some fundamental 3D structure. The folded protein must have domains, and active sites, which can exert some function, usually interacting with other proteins or with other organic molecules. In other words, there are all kinds of arguments, some of them also experimental (see for instance the interesting field of protein enineering), to believe that only a minor subset of proteins can be functional. But how minor? We have to realize that, with a search space of 10^130, even a very big number is really minor. Let's pretend, just to discuss, that 10^30 proteins of 100 aminoacids are in some way functional: they can fold in some orderly way, and they can have some biologic function, as enzymes or in other ways. 10^30 molecules would seem a very big target, and it really is. But, in a search space of 10^130 sequences, there would still be a probability of only 10^30/10^130, that is of 1:10^100, of finding that kind of target by chance in a random search. And that is still a probability vastly beyond any reasonable biologic resource (yes, I know, that's not beyond Dembski'UPB, but we have to be realistic: that kind of UPB is only an extreme reference, useful in a theorical discussion, but if we discuss real life and biological systems, probably any level around 10^30 or 10^40 is more than enough). b) But the above reasoning about "any protein which could have some function" is still only an extreme, theorical argument. In reality, given a biological context, only a very minor subset of generically functional proteins can have an "useful" function. In other words, the more a context is complex, the more a new function becomes difficult to find by chance. Let's remember that most proteins, in a cell, are functional only because they interact precisely in complex, and I would say irreducibly complex, networks of other proteins, and many of those networks are really abstract in nature: they transmit information from cell to cell or inside a cell, they regulate other functions in very finely tuned ways, and so on. Inserting a new element in such complex and finely tuned contexts really requires a very precise choice of functional proteins. So, the problem is not that a cell should give rise to any possible functional protein (which, as shown at point a) would anyway be impossible), or to the protein Dr. Dembski or anybody else defines. The cell has to find some specific functional protein which can be useful in the context of the existing biological network. A protein which can be useful in a species will not be useful in another one, and even minor differences can create enormous losses of functionality. So, given that, would you still believe that a specific organism, in a specific context, can really choose in a target of 10^30 functional proteins of 100 aminoacids (which was in itself a very generous exaggeration)? Or should we reduce the target to 10^10, or to 10^6? The real fact is that it doesn't matter. A search of 1:10^100, for all practical purposes, is as impossible as a search of 10^130, if we don't incorporate information about the desired result in the search. And the only principle which can incorporate that kind of information is design.gpuccio_{July 29, 2008
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CEC09, (25) You did mean 1200 times more generations for fruit flies than for humans, I hope. Daniel King, (21) You said,
Given appropriate assumptions, one can make any theory look ridiculous.
That depends on how you define "appropriate". If you mean assumptions chosen to embarrass a theory, that is debatable, but just barely possible for the theory of gravity and its more sophisticated relative, the general theory of relativity. Origin of life theory, however, can be embarrassed even by using rather straightforward, and even generous assumptions, as I noted here. (Comment 49. Note: read carefully before replying, to avoid personal embarrassment.)Paul Giem_{July 29, 2008
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Actually, I'm not taking into account the environmental shift of humans, and the presumably stable environment of fruit flies. This doesn't change my statement that it would be reasonable, given what we know, for there to be no de novo genes when humans and chimps are compared. It simply means that you definitely cannot take rates and percentages from one species group and use them to make estimates for a species under quite different circumstances.CEC09_{July 29, 2008
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Should we thus conclude that whereas species of fruit flies are separated by whole genes either being present or not, this isn’t the case when it comes to apes and men. Does this sound reasonable at all?
Yes. There are many more Drosophila than humans at present, and the human population has exploded only recently. It seems safe to say that the number of Drosophila has been huge throughout the past 6 million years. Furthermore, if you accept the generation rates someone gave above of 3 days for Drosophila and 10 years for humans, Drosophila have gone through about 1200 more generations over the past 6 million years than humans have. The Hawks et al. paper I linked to above would lead us to expect many fewer beneficial genetic changes in humans than in Drosophila, and it is "reasonable at all" to extend this to new genes.CEC09_{July 29, 2008
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PaV, I believe that de novo genes are genes that are not modifications of pre-existing genes. For instance, a duplication could make an additional gene, but it would not be de novo. There are a variety of patterns -- insertions, reversals, etc., which make new genes, but genes that are not de novo. If some non-coding "junk" DNA suddenly got incorporated as a working gene (not infeasible, it just needs a mutation to make a start marker, and it needs to make some functional sense) then we would have a de novo gene. However, this article says that in fruit flies about 11% of the new genes are of the de novo variety. If humans have 689 new genes, the fruit fly experience would imply that we have about 75 de novo genes. Other sources suggest that we have between 50 and 100 de novo genes. The report that we have NO de novo genes would be quite surprising in light of other reports and in light of the fruit fly study.bFast_{July 29, 2008
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Nitpicking "monkey" is nothing more than pedantry. Monkey in the context of ancestor to man is a simple, recognizable, one-word term used to describe a common primate ancestor. Given artists' renderings of what these primate ancestors looked like "monkey" doesn't seem to be particularly inaccurate. Ape-like might be a better term but who knows - the appearance of these creatures is an imaginary extrapolation from tiny bone fragments and the actual ancestry is no more than an educated guess based on age, location, and perceived similarity of bone fragments.DaveScot_{July 29, 2008
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Mr King: First, kindly inform us as to how calculations such as those summarised here are premised on dubious assumptions. Next, let us look at PaV's deductions above, as a back- of- the- envelope style, order of magnitude estimate:
As finding number 6 in the abstract, the authors write: “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.” Noting that Drosophila melanogaster has 14,000 genes (a very low gene number), the simply calculation is this: 14,000 genes/8 [NB: 8 is mid-point to [5, 11]] new functional genes per million years= 1.75 billiion years for the formation of the fly genome. This, of course, assumes that somehow the fly is ‘alive, and reproducing’ the entire 1.75 billion years—-this, without the aid of a full-blown genome. If we apply this to the monkey/human difference which, IIRC, is about a 1000 genes, then using this same rate, it would take 200 million years for man to have evolved from the monkey. This published rate for new functional gene generation cannot be good news for Darwinists.
So, kindly explain: where are the dubious assumptions in the above, and why are they dubious? GEM of TKIkairosfocus_{July 29, 2008
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"They know that if such a calculation is attempted, their theory will appear ridiculous." Given appropriate assumptions, one can make any theory look ridiculous.Daniel King_{July 29, 2008
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jdmack, (10) You said,
Darwin’s theory of evolution does not claim that man evolved from the monkey. It claims that man and monkeys both evolved from a common ancestor which no longer exists. So the observation about how long it would take for man to evolve from the monkey is not relevant to the discussion.
It is true that standard evolutionary theory assumes that chimpanzees and humans (or monkeys and humans, for that matter) descended from a common ancestor which was not a modern chimpanzee. However, until the ancestor is found, it remains hypothetical, and the ancestor could be essentially a modern chimpanzee, or the ancestor, the modern chimpanzee, and the modern human could be genetically equidistant. Even in the best-case scenario, where the ancestor is genetically precisely between modern chimpanzees and modern humans, the genetic distance between modern humans and the ancestor would still be half of that between modern humans and modern chimpanzees. Thus, the statement that "the observation about how long it would take for man to evolve from the monkey is not relevant to the discussion" is incorrect even if we replace "monkey" with "chimpanzee". The observation does not eliminate the problem; it only decreases its magnitude by half at the most. This objection reminds me of the claim that calculations cannot be made regarding the origin of life. Those making such a claim are simply trying to keep anyone from even attempting a calculation. They know that if such a calculation is attempted, their theory will appear ridiculous. Thus the spin that this area of science is beyond calculation. I guess that in these areas of science, only just-so stories are acceptable.Paul Giem_{July 29, 2008
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CEC09: From what I can see, in asserting that there are no de novo gene differences between apes and humans, Ian Musgrave seems to be giving us no more than his opinion. Notice this: the authors of the paper under discussion were working with species of fruit flies. How did they arrive at a figure for 5-11 million years for a functionally new gene to appear unless they found differences between various species of the fruit fly? Should we thus conclude that whereas species of fruit flies are separated by whole genes either being present or not, this isn't the case when it comes to apes and men. Does this sound reasonable at all?PaV_{July 29, 2008
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CEC09: (#4): I believe that a "non-functional" gene is one that is known to be transcribed---that is, m-RNA is being formed, but for which no active protein function is known to exist. So, as you allude, it's gene product is not part of the proteome. M_ackerman: (#8): Here is a citation from a Scientific American article from two years ago: "The group estimated that humans have acquired 689 new gene duplicates and lost 86 since diverging from our common ancestor with chimps six million years ago. Similarly, they reckoned that chimps have lost 729 gene copies that humans still have." This isn't the one or two a.a. differences between primates and mankind's genes. These are new, functional genes, present in the human genome, and nowhere to be found in the chimpanzee genome. New calculation: 689/~8 newly functional gene duplicates/million years= 86 million years. jdmack (#10): It is estimated that humans and chimps diverged 6 million years ago. That means that their LKCA lived 6 million years ago. I just calculated 86 million years as the needed time to account for the gene difference between apes and man. Obviously the rate published by Zhou, et. al. is problematic for Darwinists when it results in this kind of calculation. Dave1968: (#11): "Is a simple mathematical extrapolation of data obtained from an abstract really worthy of posting at Uncommon Descent?" It is when such a simple mathematical calculation doesn't jive with what is known to have happened. The whole gene duplication process, and de novo gene origination, is/are a process/es that are not fully understood. And if part of this/these process/es involve non-coding DNA, then we might be dealing with a mechanism that has very little to do with chance, and little to do with true novelty. In the meantime, prescinding from this kind of critical view, the numbers simply don't work! That's worth pointing out---even if it causes Darwinists to cringe. CEC09: I'll take a look at what Ian Musgrave has to say, but let's be realistic: just because Musgrave says there are no de novo genes separating apes and mankind, that doesn't mean he's right, or that his reasoning is right. Secondly, it is one thing for mutations to occur within genes themselves; it's an entirely different thing to have 'new genes' develop since new genes involve such a great increase in information, information coding for possibly hundreds of amino acids, and not just one or two amino acids here and there.PaV_{July 29, 2008
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By the way, don't discount the Hawks et al. article out of hand because of the fluffiness of what I cut and pasted from Hawks' blog. They actually began by making predictions based on genetic theory, and then analyzed a large amount of genetic data. They tested their claim that human adaptive evolution has accelerated against a null hypothesis, and clearly rejected the null.CEC09_{July 28, 2008
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The Zhou et al. abstract was discussed at the Panda's Thumb on June 25. Some people there were concerned about the low rate of appearance of new genes. But according to biologist Ian Musgrave, who seems to have dug into Haldane's Dilemma, there are no known de novo genes when chimps and humans are compared. See his comment for the explanation of what the differences are. This also led me to Recent acceleration of human adaptive evolution, which appeared in the Proceedings of the National Academy of Sciences in December 2007. This is an extraordinary case where you not only get full-text for free, but can read an accessible explanation by the lead author, paleoanthropologist John Hawks.
Our evolution has recently accelerated by around 100-fold. And that's exactly what we would expect from the enormous growth of our population.
His prefatory remarks make me feel not too dumb with my guessing and questioning above.
[A] very small fraction of the mutations in any given population will be advantageous. And the longer a population has existed, the more likely it will be close to its adaptive optimum -- the point at which positively selected mutations don't happen because there is no possible improvement. This is the most likely explanation for why very large species in nature don't always evolve rapidly. Instead, it is when a new environment is imposed that natural populations respond. And when the environment changes, larger populations have an intrinsic advantage, as Fisher showed, because they have a faster potential response by new mutations. From that standpoint, the ecological changes documented in human history and the archaeological record create an exceptional situation. Humans faced new selective pressures during the last 40,000 years, related to disease, agricultural diets, sedentism, city life, greater lifespan, and many other ecological changes. This created a need for selection. Larger population sizes allowed the rapid response to selection -- more new adaptive mutations. Together, the the two patterns of historical change have placed humans far from an equilibrium. In that case, we expect that the pace of genetic change due to positive selection should recently have been radically higher than at other times in human evolution.
CEC09_{July 28, 2008
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jdmack, we are not children here. We all actually understand the concept of the common ancestor. matthew_ackerman, it is my understanding that the latest count of genes unique to humans, and without apparent source (de novo) is around 50. (I read that on this blog or at TT recently, but don't have a citation.) 50 de novo genes in no more than 5 million years is a pretty good pace. Especially, consider that the lineage between man and CA probably had a generation rate of about 10 years, where the fruit fly's generation rate is a few days. 1 - We've been evolving at quite a clip. 2 - Even the fruit fly's rate of development of de novo genes seems awfully fast. I question whether its pace can be supported by statistical analysis.bFast_{July 28, 2008
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Again I ask, is there a geneticist in the house? I used to have a reminder taped to the monitor of the computer I programmed: "Don't guess!" It takes less time to look up the answer to something you're not sure about or to write a little test program to see how things actually work than to guess and straighten things out later with debugging. I feel kind of bad about guessing in my comments. I'm not lazy. The problem is that it takes some knowledge of a field to look up answers to questions in the field. I hope someone knowledgeable will point me in the right direction.CEC09_{July 28, 2008
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PaV, thank you for sending me off to read about pseudogenes. As I understand it, a pseudogene is a DNA sequence that looks much like a known gene but does not function as a gene. Do you suppose a gene is called de novo if it isn't a good match for any other known gene in the Drosophila species group? What I'm guessing is that all new genes not considered de novo arose through mutation of existing genes (changing function) or mutation of pseudogenes (introducing gene function). Does that make sense? Biologists say that the rate of evolutionary innovation differs considerably from one species to the next. Would you please explain your rationale for extending the observed rate of appearance of new genes in a particular species subgroup to quite a different species? I'm guessing that a small genetic change may yield a crucial first step into a new (maybe extended) niche. There may be many payoffs for genetic change in the new niche that are not available in the old niche. My un-expert hunch is that the rate of gene formation is related to the time a type has occupied its niche. This leads me to ask how long fruit flies have occupied their niche(s)? Many people know that the rate of genetic change in humans is high. Relatively few know that it is also high in chimps (which are apes, not monkeys).CEC09_{July 28, 2008
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Off Topic: ID skeptic D'Souza rebuts Dawkins following Al Jazeera "debate": http://townhall.com/columnists/DineshDSouza/2008/07/28/countering_richard_dawkins_on_al-jazeeraruss_{July 28, 2008
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Is a simple mathematical extrapolation of data obtained from an abstract really worthy of posting at Uncommon Descent? This seems to be the intellectual equivalent of doing a movie review based on a trailer. I wish people would stop using religious terminology (zephr) to insult Darwinists. Does that not reflect badly on religion? Does calling atheism a "religion" really hurt atheism or does it hurt religion even more by associating the negative connotations of atheism with it? The idea of a "Darwinian priesthood" is asinine. Who are you trying to insult here? Darwinists or priests? I'm sorry but some of you people really need to think about what you're saying and not just fly off the handle trying to insult atheists and Darwinists. It is more likely to hurt your cause than help it.Dave1968_{July 28, 2008
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Just one minor quibble with this blog entry (or perhaps major). Darwin's theory of evolution does not claim that man evolved from the monkey. It claims that man and monkeys both evolved from a common ancestor which no longer exists. So the observation about how long it would take for man to evolve from the monkey is not relevant to the discussion.jdmack_{July 28, 2008
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The implications of this are awesome, and thus they will be entirely and predictably ignored by the Darwinian priesthood. It's a very big problem not only for the putative hominid evolution line, but for primate and hominoid evolution across the board in all families. It's worse than that of course (for Darwinians at least) -it's a problem across the animal kingdom, and most obviously with mammalian evolution in all orders. Goes to show just how overly generous Remine is being to the Darwinians in his appraisal of Haldane's Dilemma. And even with the dice loaded in their favour, they are flummoxed.zephyr_{July 28, 2008
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