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In defense of Swamidass

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After reading Dr. Cornelius Hunter’s panning of Professor S. Joshua Swamidass’s recent article, Evidence and Evolution, I figured the professor must have written a truly awful piece. Nevertheless, I decided to go back and have a look at his article. And I’m very glad I did. Swamidass’s article was irenic in tone, easy to follow, deeply learned, and absolutely right.

Professor Swamidass’s olive branch

What Professor Swamidass was attempting to do in his article was to extend an olive branch to creationists. Nowhere in the article did he belittle or ridicule his opponents, and there was not a trace of the smug superiority which many scientists display, when talking to creationists. Indeed, he bent over backwards to be accommodating:

If we allow for God’s intervention in our history, it is possible we do not share a common ancestor with apes. Adding God into the picture, anything is possible…

Of course, adding God back into the picture, anything could have happened. An omnipotent God could have created us 6,000 years ago…

Of course, the scientific account is not the whole story. It is an open theological question how to complete the scientific account, and theological debate surrounding this question is important and engaging. One thing all should agree on; we humans are certainly more than just apes.

Nowhere in his article did Professor Swamidass argue that evolution is true, or that God made human beings via an evolutionary process. Instead, he attempted to show that the scientific evidence (taken on its own) supports human evolution, before concluding that if humans did not evolve, then theologians need to address this evidence:

Currently, it appears that, for some reason, God chose to create humans so that our genomes look as though we do, in fact, have a common ancestor with chimpanzees

It would have been very easy for God to design humans with genomes that were obviously different than apes, and clearly not a product of evolution. From some reason, He did not. He did not even make us as different from chimpanzees as mice are from rats. Why not?

Let me note for the record that young-earth creationist Todd Wood asked exactly the same question in a recent review of Fazale Rana and Hugh Ross’s revised 2015 edition of their book, Who Was Adam?:

Why do humans and chimps share such similar genomes, while the genomes of rats and mice differ so dramatically (see Mouse Genome Sequencing Consortium 2002)? What is the basis of the pattern of similarity (Wood 2006)?

…Similarity requires explanation, regardless of whether it’s similar genes or similar intergenic DNA.

Professor Swamidass draws no conclusions in his article; he merely poses a legitimate question which creationists have also wondered about. He certainly sounds like a very fair-minded man. I should add that Swamidass is a practicing Christian as well as a trained scientist. At the very least, his article warrants a courteous and carefully argued response. I regret to say that Dr. Hunter’s reply fails on this count: it is misinformed (as I’ll show below), polemical and curtly dismissive in tone, as the following extract shows:

The evolutionist has just made an unbeatable (and unfalsifiable) argument.

This is not science. Swamidass’ claim about what is and isn’t likely “without common descent” is not open to scientific scrutiny…

If Swamidass is correct then, yes, of course, the genomic data must be strong evidence for common ancestry. But it all hinges on his metaphysics. This is not about science. It never was.

Like that old baseball card, it’s just another worthless argument.

“Worthless argument”? Professor Swamidass deserves a better hearing than that.

Dr. Hunter’s criticisms of Professor Swamidass’s argument

Dr. Hunter’s failure to address the scientific evidence for common descent

Amazingly, Dr. Hunter manages to completely ignore the scientific evidence for evolution presented in Professor Swamidass’s article. Instead of addressing this evidence, he confines himself to quoting just two sentences from the article. Here’s the scientific evidence for human evolution, summarized by Swamidass, which Dr. Hunter overlooked:

In particular, be sure to check out the links to Dr. Dennis Venema’s more complete explanations of the evidence for the general public: common ancestry and genetic similarity (parts 1, 2, 3, and 4), synteny (parts 1 and 2), pseudogenes (parts 1 and 2), egg yolk (parts 1, 2, 3, and 4) and hominid evolution (hominid genetics and chromosome 2).

Evidence for human evolution: we have remnants of genes for making egg yolks

Here’s just one intriguing piece of evidence for common ancestry, which Dr. Dennis Venema writes about in a series of articles linked to by Professor Swamidass. Unfortunately, this evidence is never even mentioned by Dr. Hunter in his article:

Vitellogenins are large proteins used by egg-laying organisms to provide a store of nutrition to their embryos in egg yolk. Since vitellogenins are so large, they are a good source of amino acids when digested (proteins are made of amino acids linked together). Many of the amino acids in vitellogenins have sugars attached to them as well, so they also serve as a source of carbohydrates. The three-dimensional shape of vitellogenin proteins also acts as a carrier for lipids. As such, vitellogenins can be synthesized in the mother and transferred to the yolk as a ready-made supply of amino acids, sugars, and lipids for the developing embryo.

Placental mammals, on the other hand, use a different strategy for nourishing their embryos during development: the placenta. This connection between the mother and embryo allows for nutrient transfer right up until birth. As such, there is no need for vitellogenins, or storing up a supply in the egg yolk for the embryo to use. Evolutionary biology predicts that placental mammals descend from egg-laying ancestors, however – and one good line of evidence in support of that hypothesis (among many) is that placental mammals, humans included, have the remains of vitellogenin gene sequences in their genomes.

Dr. Hunter: we can’t say what God would or wouldn’t do

Dr. Hunter’s response to such arguments is to cry foul, on the grounds that such an argument involves an appeal to metaphysics:

A scientist cannot know that something is unlikely “without” his theory. That implies knowledge of all other possible theories. And that knowledge does not come from science.

I disagree. The scientific case for human evolution doesn’t need to specify what a Designer would or wouldn’t do. All it says is that if the Designer of life has no special reason to make X, and we discover X, then X should count as a surprising fact – and hence, a prima facie improbable one. On a special creationist account of human origins, there is absolutely no reason to expect that humans would have what appear to be the remains of genes used for making egg yolks in their DNA – just as there is no particular reason to expect that humans would be more genetically similar to chimps than rats are to mice – or for that matter, than foxes are to wolves, or horses are to donkeys. And let’s remember that most creationists consider horses and donkeys to be members of the same “kind,” just as they consider foxes and wolves to be members of the same kind, and of course, rats and mice as well (see here for a detailed discussion of kinds by Dr. Jean Lightner, from Answers in Genesis. Reasoning on Bayesian grounds, these striking and singular facts have a high probability on the hypothesis of common descent, but are surprising (and hence improbable) on a hypothesis of separate creation. One can only conclude that these facts lend scientific support to the hypothesis of common descent.

Can evolution account for the fact that humans and chimps are genetically much more similar than mice and rats?

Dr. Hunter also faults Professor Swamidass for claiming that the similarity of human and chimpanzee genomes was “predicted by common ancestry,” and that the recent scientific discovery that “humans are about 10 times more genetically similar to chimpanzees than mice are to rats” was “just as predicted by the fossil record.” Hunter replies:

First, the high chimp-human genomic similarity was not predicted by common ancestry. No such prediction was made and no such prediction is required by common ancestry. Common ancestry would be just fine with very different levels of similarity than 98-99%…

Second, Swamidass’ claim that mouse-rat divergence, compared with the chimp-human divergence, is “just as predicted by the fossil record” is also blatantly false…

In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome.

What Dr. Hunter omits to mention is that Professor Swamidass attached a lengthy footnote, which supplies the context for his remarks about rats and mice:

A common lawyerly objection to this evidence is that these similarities are “equally” explained by common “design.” As scientists, our response to this objection is data. Many modern creationists think that the genetic evidence shows that mice and rats share a common ancestor, even though they are 10 times less similar than humans are to chimpanzees. Starting from the genetic evidence, why is it hard to believe chimpanzees and humans are related (less than 1.5% codons different), when we readily accept mice and rats are related (more than 15% different)? Of course, on the outside, not looking at our genomes, humans are very different than chimpanzees, much more different than mice are from rats. Common ancestry predicts this discrepancy between function and genetics by recognizing that genomes are better explained by evolutionary history than readily observable differences between species; mice and rats are more different because they changed more quickly (because of their shorter generation time) for a longer period of time than humans and chimpanzees. What design principle can explain why humans are 10 times more similar to chimpanzees than mice are to rats? No one knows.

While Dr. Hunter is correct in pointing out that the hypothesis of that humans and chimps shared a common ancestor, taken by itself, implies nothing about their degree of genetic similarity, he neglects to mention that scientists routinely make use of molecular clocks in order to determine when two species (A and B) diverged, based on their degree of genetic similarity. They do this by using the fossil record to determine independently when two other species (X and Y) diverged, and comparing the divergence between X and Y with that between A and B, in order to calculate the date when species A and B diverged. The basic idea here is that nucleotide sequences in DNA change over time at a rate which is roughly constant across all species, as predicted by Motoo Kimura’s neutral theory of evolution, which, as Professor P.Z. Myers explains in a 2014 blog post, has been vindicated over “selectionist” theories (which categorized mutations as either advantageous or disadvantageous) by the experimental evidence:

First thing you have to know: the revolution is over. Neutral and nearly neutral theory won. The neutral theory states that most of the variation found in evolutionary lineages is a product of random genetic drift. Nearly neutral theory is an expansion of that idea that basically says that even slightly advantageous or deleterious mutations will escape selection — they’ll be overwhelmed by effects dependent on population size. This does not in any way imply that selection is unimportant, but only that most molecular differences will not be a product of adaptive, selective changes…

When comparing the rates of change between homologous genes in different species, we had a bit of a surprise: they are very roughly, sloppily constant. That shouldn’t be true under pure selection theory, but it turns out to make a lot of sense under nearly neutral theory. There is a tradeoff in the rate of mutations occurring, and in becoming fixed in a population. A very large population size will accumulate more mutations purely by chance, but the probability of a single mutation becoming fixed in the population is reduced under large population sizes. When you do the math, you discover that population size cancels out, and the frequency of novel forms becoming fixed over time is dependent solely on the mutation rate.

Think about that. If you compare two species, the number of nucleotide differences between them is basically going to be simply the mutation rate times the number of generations separating them from their last common ancestor. That’s how we can use a molecular clock to date the time of divergence of two lineages.

Professor Soojin Yi (School of Biology, Georgia Institute of Technology, Atlanta) provides a helpful summary of how scientists use molecular clocks and what their limitations are, in a recent article titled “Neutrality and Molecular Clocks,” (Nature Education Knowledge 4(2):3, 2013).

So, what do the fossils show? Sahelanthropus (pictured at the top of this post), who lived around 7 million years ago, is currently considered to be very close to the last common ancestor of humans and chimpanzees (see this family tree for a summary of changes which are believed to have occurred in the human lineage). By contrast, rats and mice appear in the fossil record at least 14 million years ago, according to the Wikipedia article on Murinae (the subfamily comprising Old World rats and mice):

The first known appearance of the Murinae in the fossil record is about 14 million years ago with the fossil genus Antemus. Antemus is thought to derive directly from Potwarmus, which has a more primitive tooth pattern. Likewise, two genera, Progonomys and Karnimata, are thought to derive directly from Antemus. Progonomys is thought to be the ancestor of Mus [the common mouse – VJT] and relatives, while Karnimata is thought to lead to Rattus [the rat] and relatives. All of these fossils are found in the well-preserved and easily dated Siwalik fossil beds of Pakistan.

For more information on the evolution of rats and mice, see here.

Is the chimpanzee really the animal closest to us?

Left: A chimpanzee mother and baby, Baltimore Zoo. Cropped image, courtesy of Wikipedia.
Right: Orangutan, Semenggok Forest Reserve, Sarawak, Borneo, Malaysia. Courtesy of Wikipedia.

Dr. Hunter’s discussion of the difficulties attending the hypothesis of human evolution is even more disappointing. He begins by attacking the claim that the chimpanzee is the creature closest to human beings:

Evolutionists believe that we humans evolved from a small ape-like creature and that our closest relative on the evolutionary tree is the chimpanzee. The chimpanzee must be our closest relative, they reason, because the chimp’s genome is closest to ours, and according to evolution, genetic mutations are the fuel behind evolutionary change.

The problem with this reasoning is that the chimpanzee is not very similar to humans according to many other measures. There are enormous differences between the two species. Furthermore, in its morphology and behavior, the orangutan is closer to humans than the chimpanzee.

A quick point about the genetic similarities between humans and chimp DNA: they really are about 98% similar, as I argued in a post last year. What’s more, even alleged de novo genes found in human beings turn out to have 98% similar counterparts in chimps.

As regards Dr. Hunter’s claim that humans are morphologically more like orangutans than chimpanzees, I’m afraid he’s relying on out-of-date information here. Back in 2009, Professor Jeffrey Schwartz and Dr. John Grehan generated a brief flurry of controversy in the scientific world when they published a paper which listed 63 physical characteristics which had been verified as unique to humans and other great apes – chimps, gorillas, and orangutans – and discovered that humans shared no less than 28 of these characteristics with orangutans, but that they only shared two characteristics with chimpanzees, seven with gorillas, and seven with all three apes (chimpanzees, gorillas, and orangutans). Dr. Schwartz has long argued that our closest relative is the orangutan (from whom he says we diverged 12 or 13 million years ago), and he contends that the genetic data don’t tell the whole story, because most human-chimp comparisons only look at the coding region of the human genome. However, in 2010, another team of researchers (Lehtonen et al.) redid the research, using a much larger set of 300 anatomical features, and found (with a 98% degree of confidence) that the ape most similar to human beings was the chimpanzee, after all. Grehand and Schwartz hit back with a paper of their own in 2011, in which they argued that Lehtonen et al. shouldn’t have counted some of the anatomical features listed in their study, but Lehtonen et al. replied with an article showing that Grehan and Schwartz were guilty of logical inconsistencies in their methodology. In other words: evidence purporting to show that humans are physically more like orangutans than chimpanzees turned out to be highly questionable, and there’s no good reason to doubt that chimpanzees are the apes which are closest to human beings – although recent evidence suggests that the common ancestor of humans and chimps may have walked like an orangutan. However, I don’t blame Dr. Hunter for accepting the claim that humans are anatomically closer to orangutans than to chimps: at one point, I was taken in by it myself.

If even the evolution of proteins requires a Designer, how much more so does human evolution

Dr. Hunter continues:

According to evolution, you can’t have mutations occurring for some purpose, such as creating a design. And natural selection doesn’t help — it cannot induce or coax the right mutations to occur. This makes the evolution of even a single protein, let alone humans, statistically impossible.

In this passage, Dr. Hunter is alluding to the pioneering work of Dr. Douglas Axe, the author of the 2010 paper, The Case Against a Darwinian Origin of Protein Folds, which I blogged about here. See also here, here and here for follow-up comments by Dr. Axe and Dr. Ann Gauger, in response to criticisms. As far as I can judge, evolutionists have failed to mount a substantial challenge to Dr. Axe’s arguments demonstrating the astronomical improbability of certain protein folds which are essential for all living organisms having evolved by unguided processes. So I am in complete agreement with Dr. Hunter that human beings did not get here by either a chance process or by natural selection.

However, Professor Swamidass never claims in his article that human beings originated via a blind process. As I mentioned above, he’s a scientist who is a Christian. His sole aim, in writing the article, was to show creationists that there is a wealth of scientific evidence supporting the claim that human beings and chimpanzees shared a common ancestor. Nothing in that claim stipulates the mechanism whereby humans arose: it may have been a guided process or an unguided one.

The mystery of human consciousness

Next, Dr. Hunter argues that evolution cannot account for the mystery of human consciousness:

The incredible designs in the human body are not the only thing those random mutations have to create—they will also have to create human consciousness.

Evolutionists may try to explain consciousness as an “emergent” property that just luckily arose when our brain somehow evolved. Or they may try to explain that consciousness is really no more than an illusion. But these are just more demonstrations of anti-realism in evolutionary thought. Evolutionary theory constructs mechanisms and explanations that do not correspond to the real world. So this is another problem Swamidass will need to overcome.

However, nowhere in his article does Professor Swamidass attempt to argue that evolution can explain human consciousness. All he is endeavoring to demonstrate is that there is strong scientific evidence that humans and chimps had a common ancestor. Remember: the guy is a Christian, not an atheistic reductionist.

Can the relatively tiny modifications of an ape-like ancestor’s genome account for the vast differences between humans and chimps?

Dr. Hunter ridicules the notion that the morphological differences between humans and chimps can be explained by a relatively small number of modifications in their ancestors’genomes, when species that have undergone much greater genetic modification display far fewer morphological differences:

In recent decades the genomes of humans and chimps have been determined, and they make no sense on evolution. One of the main problems is that the genes of the two species are almost identical. They are only about 1-2% different and, if you’re an evolutionist, this means you have to believe that the evolution of humans from a small, primitive, ape-like creature was caused by only a tiny modification of the genome.

This goes against everything we have learned about genetics. You can insert far greater genetic changes with far less change arising as a consequence. It makes little sense that tiny genetic changes could cause such enormous design changes to occur.

Dr. Hunter’s argument is flawed, because he overlooks the fact that the vast majority of genetic changes are now known to be either neutral or nearly neutral, as explained above: they are product of random genetic drift, and they are mostly non-adaptive. By contrast, morphological changes (including the “design changes” referred to by Dr. Hunter) are often subject to natural selection, which means that they may be either beneficial or deleterious. Consequently, the degree of genetic divergence between two species tells us little or nothing about how different they are, morphologically. That explains how the morphological differences between rats and mice can be relatively slight, even though rats and mice are believed to have diverged long before humans and chimps (which are so morphologically dissimilar that they were placed in separate families until scientists discovered how similar they were genetically).

It has been calculated (Arbiza, 2006; Yu 2006; Donaldson & Gottgens 2006; Kehrer-Sawatzki & Cooper 2007) that a mere 340 beneficial mutations would have been sufficient to transform the common ancestor of man and chimp into a human being, according to biologist Ian Musgrave of Panda’s Thumb. (That’s 240 mutations in protein-coding genes and 100 in regulatory genes.) By contrast, the number of (mostly neutral) mutations occurring in the human lineage is thought to have been about 22.5 million. In other words, the neutral mutations in our lineage outnumber the beneficial mutations by about 100,000 to 1. The vast majority of genetic differences between humans and chimpanzees have nothing to do with survival, or evolutionary fitness.

Could 340 beneficial mutations have been enough to make us human?

Dr. Hunter is aware of this argument, but he doesn’t find it convincing:

Not only is evolution limited to tiny genetic modifications to create the human, but the majority of those modifications would have had to be of little or no consequence…

…[The authors of a 2005 paper on the chimpanzee-human genome comparisons] were forced to conclude that most of the mutations affecting protein-coding genes led to “neutral and slightly deleterious alleles.” So not only are evolution’s random mutation resources meager, in terms of both quality and quantity as explained above, but even worse, those mutations mostly led to “neutral and slightly deleterious alleles.”

That’s right. According to current evolutionary thinking, most of the mutations separating us from chimps were inconsequential, from a survival perspective. A relatively small number of changes – in fact, a mere 340 – made all the difference.

Now, you might be inclined to say: “That’s ridiculous!” Fine. My response is: prove it. You can’t just rely on intuition, because intuition is not infallible. To illustrate my point, consider a transition which dwarfs even the metamorphosis from an ape-like creature to a human being: the transformation from a land animal to a whale. Ask yourself: how many steps would have been required to accomplish this change? Biochemist Larry Moran has an answer for you: “Evolutionary biologists who have spent their entire careers studying evolution, genetics, and developmental biology are comfortable with a few thousand mutations causing the transformation from land animals to whales.” Crazy? That’s what I thought too, when I saw the figure. But if you do the calculations, it turns out that a few thousand mutations might be enough after all, for reasons I discussed in a recent post.

Is there any evidence for natural selection operating on the human brain?

Next, Dr. Hunter argues that the only evidence for natural selection in the human genome relates to relatively trivial functions like smell and hearing, and that there’s no evidence for natural selection operating on the human brain:

When evolutionists search for genes in the human genome that do show signs of selection, rather than neutral drift (again, under the assumption of evolution), they find only a limited repertoire of functionality. For example, one study found genes involved in the sense of smell, in digestion, in hairiness and in hearing. In other words, evolution is suggesting that we differ from the chimp mainly in those functions. It is a silly conclusion and another problem for Swamidass to explain.

Dr. Hunter neglects to inform his readers that the study he cited is a very old one: it goes back to 2003. What’s more, the study included an important disclaimer: “This study has focused only on protein-coding genes, and it will require examination of regulatory sequences to determine the contribution of regulation of gene expression to the evolutionary divergence between humans and chimps.” A more recent paper by Capra et al., published in the Philosophical Transactions of the Royal Society B in 2013, reveals that out of the 2649 non-coding human accelerated regions (ncHARs) which they analyzed in the human genome, about 30% (or 773) function as developmental enhancers, and that using a prediction tool known as EnhancerFinder, the scientists predicted that “251 of the 773 ncHAR enhancer candidates are active in brain development, 194 are active in limb development and 39 are active in heart development.” It turned out that among the validated enhancers, brain enhancers were actually the most common. So much for Dr. Hunter’s claim that the functions identified by scientists in which humans differ from chimps mainly relate to the sense of smell, digestion, hairiness and hearing.

A molecular clock that ticks at different rates in different regions of the human genome

But Dr. Hunter has more up his sleeve. This time, he quotes from a paper dating back to 2005, which found that nucleotide divergence rates are not constant across the human genome. In other words, the molecular clock ticks at a different rate at different places:

That 2005 paper also found a host of chimp-human comparisons that are nonsensical on evolution… For example, if you look at large segments of DNA, which are corresponding in the human and the chimp, you find unexplainable variations in the chimp-human differences…The usual explanatory devices do not work, so evolutionists are left only with the claim that local variations in the mutation rate did it—which amounts to special pleading…

Hang on a minute. How big are the differences we’re talking about here? Are we talking about a ten-fold difference between divergence rates across the genome? Nope. Not even close. A five-fold difference, perhaps? Wrong again. To see what Dr. Hunter is talking about, take a look at this graph. It shows that the overall difference between human and chimp DNA is about 1.2%. If we compare different chromosomes, we find that the difference is slightly higher on some chromosomes than others. And that’s all. If we look at the median figures for chromosome pairs 1 to 22, we find that the genetic difference between humans and chimps varies from about 1.1% to a little under 1.4%. The authors were a little surprised that there was even that much variation, and they wrote: “The average divergence in 1-Mb segments [of the genome – VJT] fluctuates with a standard deviation of 0.25%, which is much greater than the 0.02% expected assuming a uniform divergence rate.” To recap: the study’s authors reported that the mean divergence between human and chimp DNA is 1.2%, and if the molecular clock ticked at a uniform rate across the genome, then the authors would have expected relatively slight variations in this divergence. Instead, they found fluctuations with a standard deviation of 0.25%, which is still insignificant compared to the mean divergence of 1.2%. In other words: so what? Dr. Hunter is making a mountain out of a molehill.

Local variations in the genetic divergence rate between humans and chimps

Dr. Hunter continues:

The supposed divergence rate between chimps and humans not only has an unexplainable variation in large, 1-Mb segments of DNA, it also has an unexplainable variation towards the ends of most chromosomes. This is another problem that seems to make no sense on evolution, which Swamidass must explain.

But that’s not all.

This supposed divergence rate between chimps and humans also has an unexplainable variation that correlates with chromosomal banding. Again, this makes no sense on evolution. Why should the chimp-human divergence vary with the banding pattern? Evolutionists have only just-so stories to imagine why this would have happened, and it is another problem for Swamidass to address.

So, how much of a variation are we talking about here? If we look at the graph provided by the authors of the study, we see that even near telomeres (the ends of chromosomes), the level of divergence between human and chimp DNA never gets above 2.1%, and elsewhere in the genome, it never falls below 1.0%. In other words, we’re talking about a two-fold variation in the rate at which the molecular clock ticks, in the worst possible case. Earth-shattering, isn’t it?

Dr. Hunter wonders why the level of chimp-human genetic divergence would vary with the chromosomal banding pattern, and why it would be higher near the ends of chromosomes, if humans evolved. Short answer: I don’t know, and neither do the study’s authors. But I’d like to ask Dr. Hunter a question: can he account for these facts, on a creationist account of origins? He can’t. In other words, what we have is a curious fact which neither evolution nor creation explains well, and which is fatal to neither theory – or putting it more succinctly, much ado about nothing.

Can evolution account for the dissimilarities in rat and mouse genomes?

But Dr. Hunter thinks he has another ace up his sleeve: the fact that the genetic difference between mice and rats is about 10 times greater than that between humans and chimps.

This supposed divergence rate between chimps and humans is not consistent with the supposed divergence rate between the mouse and rat. The mouse-rat divergence is about an order of magnitude greater than the chimp-human divergence. And yet the mouse and rat are much more similar than the chimp and human. It makes no sense on evolution. In fact, before the rat genome was determined, evolutionists predicted it would be highly similar to the mouse genome…

The prediction that the mouse and rat genomes would be highly similar made sense according to evolution. But it was dramatically wrong.

Dr. Hunter is right on one point: scientists were at first surprised to discover that the genetic difference between rats and mice was so large. That’s because they based their prediction on the morphological differences between rats and mice, which are relatively small, and inferred that the genetic difference would be small, too. That was a big mistake, for reasons explained above: the vast majority of the genetic differences between any two species are neutral or near-neutral mutations, which dwarf beneficial mutations by a factor of about 100,000 to 1. However, the fossils tell a different story: rats and mice diverged at least 14 million years ago, compared with 6 or 7 million years for humans and chimps. And when scientists calculate the time of divergence using genetic differences, they arrive at a median figure of 17.9 million years ago for the date when rats and mice diverged, versus 6.2 million years ago for the split between humans and chimps, according to timetree.org. I’d say that tallies reasonably well with the fossil record. And I don’t say that lightly: I have in the past been highly critical of inconsistencies in the molecular clock, which I highlighted in a post written four years ago. There is still a lot we don’t know, and alert readers will have noticed that current estimates of the date when humans and chimps diverged vary considerably, as this graph reveals. Nevertheless, the vast majority of the estimates lie between four and nine million years ago, so we’re talking about a two-fold variation, which is still far less than even one order of magnitude. That’s annoying, but scientists can live with it, just as astronomers back in the 1970s and 1980s were able to live with the fact that the age of the universe lay somewhere between 10 and 20 billion years, depending on the method you used to measure it. (They’ve now concluded that it’s 13.8 billion years old.)

Dr. Hunter’s last stand

But Dr. Hunter believes he has one more argument that will demolish the case for human evolution:

The mouse-rat divergence date is estimated by evolutionists to be older than the chimp-human divergence date. Furthermore, the lifespan and generation time for mice and rats are much shorter than for chimps and humans. From this perspective, and given these two effects, one would conclude that the mouse-rat genetic divergence should be much greater—at least two orders of magnitude greater—than the chimp-human genetic divergence. But it isn’t. It is only about one order of magnitude greater.

Wrong. As we’ve seen, mice and rats diverged around 18 million years ago, compared with around six million years ago for humans and chimps. That’s a three-fold difference. What about the effects of generation time on the molecular clock? Soojin Yi addresses this point in her 2013 paper, “Neutrality and Molecular Clocks,” which I cited above:

Wu & Li (1985) were the first to test the generation-time effect hypothesis using DNA sequence data. They used data from 11 genes of primates and rodents. Since primates have a much longer generation time than rodents do, the molecular clock should be faster in rodents compared to primates. Indeed, they found that for synonymous sites, rodents show approximately two times the rate of molecular evolution when compared to primates (Wu & Li 1985). For nonsynonymous sites however, such an effect was not found. In other words, the neutral molecular clock, but not the amino acid molecular clock, ticks faster in the rodent lineage compared to the primate lineage, which fits well with the idea of a generation-time effect.

So the neutral molecular clock ticks twice as fast for rats and mice as it does for primates. Multiply that by the three-fold difference between the 18-million-year-old mouse-rat divergence date estimated by evolutionists and the 6-million-year-old human-chimp divergence date, and you get an expected level of genetic divergence which is just six times greater – and not two orders of magnitude (or 100 times) greater, as calculated by Dr. Hunter. This figure of a six-fold difference comports well with the ten-fold genetic divergence reported by Professor Swamidass in footnote 2 of his article: at least 15% of the codons in rats and mice are different, compared with less than 1.5% in humans and chimps.

Conclusion

There is a lot that we still don’t know about human origins. I accept that. But it would be foolish to deny that the scientific evidence points clearly to our having shared a common ancestor with the chimpanzee. Such a conclusion is in no way at odds with Intelligent Design.

What do readers think?

UPDATE:

Readers may wish to peruse the following articles, written in response to my post and to Professor Swamidass’s article, “Evidence and Evolution”:

A Response to VJTorley by Dr. Cornelius Hunter.
One Long Argument — Responding to VJ Torley on Human-Ape Common Descent by Dr. Cornelius Hunter.
Of Tree Rings and Humans by David Klinghoffer.
Debating Common Ancestry by John West.

Professor Swamidass has also written a follow-up article:
Call for Response to the Tree.

I also wrote a short comment in response to Professor Swamidass’s article, “Evidence for Evolution”, which has recently been updated with an FAQ section:

Hi Dr. Swamidass,

Thank you very much for your kind remarks about my post on Uncommon Descent.

I’d just like to comment briefly on what you said about Dr. Hunter in the FAQ:

“Third, I do believe that Dr. Hunter is not being intentionally deceptive or manipulative. I believe he is making a good faith effort, to the best of his abilities, to engage the evidence I have raised.”

I would like to endorse what you said. I pulled no punches in my post, and on a few occasions, I did criticize Dr. Hunter for relying on flawed arguments. I also wrote that he “neglects to inform” his readers on a couple of basic points. For the record, I wish to make it quite clear that I am not accusing Dr. Hunter of being intentionally deceptive. All of us are, at times, guilty of an unintentional bias towards arguments that we personally favor, and it is all too easy to ignore what we might perceive as very minor or trivial problems in these arguments, when presenting them to an audience. That was what I had in mind when I wrote about Dr. Hunter’s “neglect.”

Despite my differences with Dr. Hunter, I have the greatest respect for him as a Christian, and I would like to thank him for his forbearance and courtesy.

Likewise, when I referred to Dr. Hunter in my post as believing he had an ace up his sleeve, I was not implying that he was resorting to any sleight-of-hand or trickery. Rather, I was using the term in the sense in which the Cambridge English dictionary defines it: secret knowledge or a secret skill that will give you an advantage.

For the record, I believe Dr. Hunter to be an honest man. And I apologize for any pain or distress suffered by Dr. Hunter as a result of reading my post. I wish him well.

Comments
gpuccio @95
Alternative splicing is certainly an important factor. But the problem is: what controls alternative splicing? We often take alternative splicing for granted, but we need to understand how different forms of s proteins can have different functions, what guides cells to effect the correct splicing at the correct time, and so on. IOWs. the problem is always: what information guides alternative splicing, or other epigenetic strategies, like histone modifications, DNA methylation, and so on? In the end, most differences must explain how cell behave, how they differentiate, how they find their place and role, how they build macroscopic forms and body plans. And we still understand very little of all that.
Excellent point.Dionisio
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Very interesting discussion. Keep it up! :)Dionisio
May 15, 2016
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bill cole: I agree. Please, consider that I am a convinced defender of biological ID in its strongest form: for me, RV + NS cannot explain even a single functional protein, least of all a new species, least of all humans! :) Anything which exhibits more than 150 - 500 bits of digital functional information (we can discuss the safest threshold) is IMO designed.gpuccio
May 15, 2016
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Hi gpuccio
If you prefer to think that the apes-humans transition is special, I have no problem with that. I think that too, but the “special” for me is linked to other considerations, and not in particular to the problem of CD.
I am trying to get scientific clarification. The public has been lead to believe that this transition by understood natural means is a fact. Based on our discussion I think that you agree this is not at all a fact and almost certainly wrong. I think CD became a confusing term once we no longer considered RMNS the driver of evolutionary change. I applaud Mung's attempt to clarify and your subsequent agreement :-)bill cole
May 15, 2016
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Mung: Descent with designed modifications is very good for me! :)gpuccio
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bill cole: I have tried to explain why I accept CD (not "claim" it) as a reasonable explanation. The transition from apes to humans is certainly one of the most difficult issues. For me and my arguments, it is not more important than any other transition in natural history, but I can understand the importance it has for other reasons. If you prefer to think that the apes-humans transition is special, I have no problem with that. I think that too, but the "special" for me is linked to other considerations, and not in particular to the problem of CD. However, my reasonings about CD are motivated by the whole scenario of genomes and proteomes throughout natural history, and they do not depend particularly on the apes-to-human transition. If it were shown that for some reason that transition is an exception, I would still accept CD as a general principle of biological design.gpuccio
May 15, 2016
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mk: I appreciate your arguments. Here are my answers: "first- how we can be sure?" In science we are never sure. We just try to choose the best explanation with what we know. That is an essential part of my scientific epistemology. See my post #51. "secondly- about the h4 protein. i know about one experiment showing that we can delete a big part from the protein and it still remain functional. so it may not be conserve after all." I definitely disagree with that conclusion. I know that paper. You cannot really evaluate functionality in those terms. True functionality is proven in the wild, and in long times. The paper you refer to, IMO, does not prove in any way that the conservation of histone sequence is not due to functional constraints. If you give me the reference for it again, we can discuss the paper in more detail. "3-i think about this example: according to evolution fly and mosquito split off about 250 my ago. fly generation is about less than one month. so even if one generation mean only 1 new mutation we will need only 10^8 month to change his entire genome. or about less than 10^7 years. so fly and mosquito are suppose to be different in about their entire genomes from each other. far from reality. it may be evidence that most of the dna sequence is functional and not neutral." I definitely agree with you on that. I do believe that most of the genome is functional. But, at the same time, much of the functional genome is tolerant to some variation. We have good evidence of that in proteins, even in human proteins, for example in polymorphisms which do not affect function or cause disease, which are very frequent. Neutral variation exploits that tolerance. In functional non coding DNA, that tolerance could even be greater. "last problem is that we cant know for sure how the original sequence look like. so we cant know what is the real Ka/Ks ratio unless we assume that evolution is true." This reasoning is not epistemologically correct, IMO. I would reason this way. We have a definite pattern of Ka, Ks and Ka/Ks ratio. That is an observable fact, and we have to try to explain it. That's what science is about. Now, we look at the relationship between that pattern and other observable facts, or other reasonable inferences, like the classification of biological beings and what we reasonably know about natural history. We are making no special assumptions here. Then, we observe definite relations between the pattern of Ka/Ks and other informations, like the chronological times of appearance of species, or their collocation in some reasonable classification of species. To explain the data I have mentioned, we propose Common Descent and neutral variation. We are not "assuming" evolution, whatever you mean by that word. We are explaining observed facts with a theory. Which is exactly what science should do. "also remember that about 30% of the genes between gorila and human are closer then chimp and human." I have no special idea about the relationship between gorilla and humans as compared to chimp and humans. I don't even consider it a very important issue, and it is certainly an issue about which I know very little. I know form my experience at blasting proteins that primates have definitely the highest protein homologies with humans. That is very difficult to deny. I accept that we are more related to primates than, say, to rodents, or even more to bony fishes, because the molecular evidence is overwhelming. And each time I have tried a Ka/Ks analysis, I have found results perfectly compatible with the gross natural history as we understand it. I have no doubts that if one tries to go more into details, more difficulties arise. That is perfectly natural. But, to prove my point, I only need the results that I can get from scenarios where the difference is more significant and easy to observe. Remember, my purpose is to show the reasons to believe in Common Descent and neutral variation in a strong ID perspective, not to build a precise tree of life. I am not interested in that.gpuccio
May 15, 2016
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gpuccio
We often take alternative splicing for granted, but we need to understand how different forms of s proteins can have different functions, what guides cells to effect the correct splicing at the correct time, and so on. IOWs. the problem is always: what information guides alternative splicing, or other epigenetic strategies, like histone modifications, DNA methylation, and so on?
Yes:-) The codes are not well understood and therefore this transition is not well understood yet we claim common decent? Aside from DNA similarities this is looking like the most dramatic transition if you look at alternative splicing data and timing data in all vertebrate evolution.bill cole
May 15, 2016
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Mung: Of course, I do believe that some of the differences are due to different functional requests. That is exactly what is usually overlooked in traditional evolutionary reasoning. So, IOWs, when we compare two homolog proteins in two distant species, we can find: 1) Identities and similarities, which must be interpreted as conservation of information due to functional constraints (negative, purifying selection). 2) Neutral differences, which can be generically divided into: 2a) Synonimous mutations in the gene, which do not modify the AA sequence in the protein, and are assumed to be neutral (with some exceptions) 2b) Mutations which do affect the AA sequence in the protein, but which are probably neutral because they do not really affect the structure and function of the protein itself. 3) Differences which correspond to different functionalities in the two species. Now, while it is certainly easy to evaluate 1) and 2a), it is really difficult to differentiate between 2b) and 3). IMO, most of 3) is usually conflated with 2b), as I have tried to argue in my post #86 to VL. In my past OPs, I have also tried to argue that regulatory proteins, or regulatory parts of proteins, are more likely to change greatly even between not so distant species, and probably contribute to different regulatory procedures: see for example my OPs about prickle protein. Proteins which have more a "final effector" role are more likely to remain similar for the functional part, and to change mainly because of neutral variation (2b). That should be the case for myoglobin, for example. You can easily understand that I believe that variation of the 3) kind is the most interesting for us, and is very reasonably designed.gpuccio
May 15, 2016
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Mung: "How can we test the claim that the differences are due to neutral mutations and that the identities are due to selection?" The Ka/Ks analysis is a way. Look at my post #89. It is generally true that in functional protein coding genes non synonimous mutations are rarer than synonimous mutations. The classical explanation is that non synonimous mutations are "antagonized" by negative selection, at least when they affect the function of the protein. On the other hand, synonimous mutations are apparently mostly unaffected, and they are grossly proportional to the time separation between the molecules. I find that explanation perfectly reasonable, and I accept it. I am not aware of any convincing alternative explanation for that pattern.gpuccio
May 15, 2016
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hi again gpuccio you said: "It is true that synonimous mutations can sometimes have functional consequences, but that is not the general rule. "- first- how we can be sure? secondly- about the h4 protein. i know about one experiment showing that we can delete a big part from the protein and it still remain functional. so it may not be conserve after all. 3-i think about this example: according to evolution fly and mosquito split off about 250 my ago. fly generation is about less than one month. so even if one generation mean only 1 new mutation we will need only 10^8 month to change his entire genome. or about less than 10^7 years. so fly and mosquito are suppose to be different in about their entire genomes from each other. far from reality. it may be evidence that most of the dna sequence is functional and not neutral. last problem is that we cant know for sure how the original sequence look like. so we cant know what is the real Ka/Ks ratio unless we assume that evolution is true. also remember that about 30% of the genes between gorila and human are closer then chimp and human.mk
May 15, 2016
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bill cole: Alternative splicing is certainly an important factor. But the problem is: what controls alternative splicing? We often take alternative splicing for granted, but we need to understand how different forms of s proteins can have different functions, what guides cells to effect the correct splicing at the correct time, and so on. IOWs. the problem is always: what information guides alternative splicing, or other epigenetic strategies, like histone modifications, DNA methylation, and so on? In the end, most differences must explain how cell behave, how they differentiate, how they find their place and role, how they build macroscopic forms and body plans. And we still understand very little of all that.gpuccio
May 15, 2016
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Mung
Perhaps we should cease to speak of common descent and speak of descent with modification. That might help distinguish the arguments, whether they are against shared descent or whether they are concerned with the means of modification.
Very good point :-)bill cole
May 15, 2016
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gpuccio VJT
bill cole: I am puzzled like anyone else by the apparent contradiction between phenotypic differences between humans and chimps (which are huge) and the small differences at nucleotide level. I have tried to comment on that in the last part of my post #78.
How much of a role do you think alternative splicing may play in this. According to the paper I recently attached the splicing codes were 30% different between the lowest level vertebrates and chimps and a 50% jump between chimps and man. Alternative splicing is an interesting "design" strategy to make large changes to proteins with a lot less code.bill cole
May 15, 2016
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Perhaps we should cease to speak of common descent and speak of descent with modification. That might help distinguish the arguments, whether they are against shared descent or whether they are concerned with the means of modification.Mung
May 15, 2016
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gpuccio:
I insist that common descent and neutral variation remain the best explanation for such a pattern, in a protein which retains essentially the same structure and function. I am ready to discuss other explanations, if you have them.
How can we test the claim that the differences are due to neutral mutations and that the identities are due to selection?Mung
May 15, 2016
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How does one picture such an event? How does one picture the subsequent diversification of life from a few animals which came off an ark after a global flood? Most creationists I know of accept at least some form of common descent even if they reject the idea that man and apes share a common lineage.Mung
May 15, 2016
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mk: In my answer at post #81 I write:
Histones are among the most conserved sequences in eukaryotes. That means that functional constraints here are extremely strong. IOWs, almost all the sequence is functional. But most proteins are much less conserved. Look for example at my nunbers for myoglobin, in post #68. It is true that synonimous mutations can sometimes have functional consequences, but that is not the general rule. Most synonimous mutations are neutral, and that’s why you find them in conserved proteins, and when you compute the ka/ks ratio in a very conserved protein, its value is very low.
To prove my statement with facts, I have blasted Histone H3 human against yeast. Both molecules are 136 AAs long. As already said in post #88, the AA sequence in the two molecules is almost identical: 121 identities, 248 bits. I have performed a computation of the Ka/Ks value between the two molecules: the result is 0.009766106. Now, as you may know, a Ka/Ks ratio around 1 points to neutral variation. A lower value points to purifying (negative) selection: IOWs, the sequence is conserved, and synonimous mutations are more frequent than non synonimous mutations, because non synonimous mutations have probably been eliminated ny negative selection, while synonimous mutations, being usually neutral, are tolerated. Here the value is 0.0097, a very low value: that confirms that the sequence is highly conserved, as we already knew. But it also confirms that even in such a conserved molecule, synonimous mutations have indeed taken place: that's why the value of Ka/Ks ratio is so low. In detail, the rate of non synonimous mutations (Ka) is 0.09766105, while the rate of synonimous mutations (Ks) is 9.999999. Those numbers prove that synonimous mutations go on even in extremely conserved sequences. That can be explained only by the fact that they are usually neutral. Remember, human vs yeast, we are discussing a probable time split of at least 1 billion years.gpuccio
May 15, 2016
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Origenes: Yes, maybe it's only a verbal misunderstanding. For me CD means only that engineering happens in existing living beings, and that what is not re-engineered is transmitted from one species to another. That is more than enough to explain the molecular data I have mentioned. Of course, new information is added when the engineering takes place, either as transformation of what exists or as addition of new content. That new information can be added gradually or suddenly: that is not really relevant, and only future data could help answer that. However, when it is added, it becomes part of what is transmitted from that point on. So, we share genes with bacteria (for example the components of ATP synthase), and some of them retain high identity. Other genes appear in eukaryotes, and we share them with fungi, for example. Other genes appear for the first time in vertebrates. And so on. The point is: our beta chain of ATP synthase, 529 AAs, shares 334 identities with the corresponding molecule in E. coli, for a total of 663 bits of functional information conserved for billion of years. I don't believe for a moment that the molecule has been re-written from scratch for each new species in 4 billion years. I believe that the molecule, with its functional information, has simply passed from one species to the other. The same comparison, made with S. cerevisiae (yeast), an eukaryote, gives 476 identities, 958 bits. The point is, even these extremely conserved molecules change a little with time, while retaining their function. And the change is grossly proportional to the separation in time between species, Isn't that perfectly compatible with CD and neutral variation in time? How can we explain that differently? Of course, histone H3 appears in eukaryotes, and remains strongly stable up to humans: Histone H3 (136 aas): human to S. cerevisiae: 121 identities, 248 bits. Myoglobin, instead, as explained, changes very much just in vertebrates. Functional constraint and neutral variation are two forces constantly opposing each other. The field for that opposition is offered by some physical continuity of living beings (Common Descent).gpuccio
May 15, 2016
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Gpuccio: No, no! I must miss something about what you think. Why do you believe that “Those new genes won’t fit well with common descent”? I don’t understand.
Because those new genes — genes written “from scratch” — don't have ancestral genes. Are we talking past each other?Origenes
May 15, 2016
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VJ: We have been making parallel discussions here, but I think we agree on many things. :) Just a question. I see from your post #74 that you accept the idea that 22.4 million mutations have probably taken place in the human line since it diverged from the line leading to chimps (and I can agree). But you also accept that these would mostly be entirely natural changes. So, you restrict the beneficial (functional) mutations to about 340. I ask: why? Isn't it more credible, if we accept the intervention of design, that many more mutations are functional? After all, those numbers are derived assuming that no design intervenes. If you consider design as a true factor, then everything changes. Most of designed mutations would naturally be in regulatory networks, IOWs, in those parts of the genome that control epigenetic procedures. As we don't know what those parts are, and how they work, those highly functional mutations would easily be classified as "neutral", simply because they take place in parts of the non coding DNA whose function we don't understand. I believe that many more mutations in humans are functional. And still even that is not enough, IMO, to explain the huge functional information which makes humans different from chimps. One of my recurrent points is that current theories definitely underestimate the diversity between species which is functional. Almost all diversity which is not in protein coding genes is usually interpreted as neutral.But species which are different must have different epigenetic procedures. And those procedures must be written somewhere. Information does not appear by magic out of thin air!gpuccio
May 15, 2016
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bill cole: I am puzzled like anyone else by the apparent contradiction between phenotypic differences between humans and chimps (which are huge) and the small differences at nucleotide level. I have tried to comment on that in the last part of my post #78.gpuccio
May 15, 2016
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Andre: I am happy that we agree on that. I love the idea of guided mutations, but I love even more the idea of guided variation through guided transposon activity. There is increasing evidence of transposon signatures in new genes.gpuccio
May 15, 2016
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Origenes: "If I understand you correctly, the reasoning goes like this: the sequence was infused as non coding in an ancestor, so it doesn’t really count as infusion of new information and therefore we won’t have to reject the concept of CD. Please correct me if I’m wrong, but such attempts to push the problem back one level, seems to me like an elaborate attempt to square infusion of new information with CD." No, no! I must miss something about what you think. Why do you believe that "Those new genes won’t fit well with common descent"? I don't understand. And why do you say that: "the sequence was infused as non coding in an ancestor, so it doesn’t really count as infusion of new information and therefore we won’t have to reject the concept of CD" No. It certainly counts as infusion of new information. The information will be activated later, but it is certainly infused before the activation. My simple point is that CD remains true. Windows 10 is "descended" from Windows 8, for example, even if massibe new information has been infused in the new version. But still, the programmers did not write everything from scratch. They took Windows 8 and re-wrote parts, and added new parts. But, for example, if there was a bug in some part of the software and it was not corrected or re-written, then you can find the same bug in Windows 10. That's how you distinguish between two software products which are derived one from the other, and two which have been written in a completely independent way. CD just means that the designer works starting from what already exists, and re-uses part of what already exists, while transforming the rest, or just adding new parts. If the engineering takes place "in vivo", by intervention on existing beings that reproduce, you have descent anyway, but it is guided descent.gpuccio
May 15, 2016
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hi vjtorley. there is several problems with their paper. for example: "However, it cannot be denied that there are numerous similarities between Homo and Pongo in morphological, life history, physiological, behavioural and cultural traits If the currently accepted hypothesis of hominid evolution is correct, these similarities must either be symplesiomorphies (shared primitive characters), convergences, or erroneous observations" so when we see a phylogenetic-morphologic contradiction they may solve this by "convergent evolution". they also cant explain other thing. for example: " Grehan & Schwartz (2009) demonstrated that the human–orangutan hypothesis provides a more parsimonious biogeographical scenario than the human–chimpanzee hypothesis, and argued that this provides external support for their phylogeny" so it isnt so simple. more then that: we know that both gorila, chimp and orang are apes. when human isnt. so in general morphological terms chimp need to be more close to gorila or orang then human. even if we ignore all this points its still doesnt evidence for a commondescent. its just mean that similar morphology=similar genome.mk
May 15, 2016
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mk: I will try to answer your two questions: 1) "the histone h4 protein sequence havent change for about 1 bilion years. so it may be true that most of the aa sequence is functional. even in the dna level we know that a codon that code for the same amino acid can have other result in the protein regulation." Histones are among the most conserved sequences in eukaryotes. That means that functional constraints here are extremely strong. IOWs, almost all the sequence is functional. But most proteins are much less conserved. Look for example at my nunbers for myoglobin, in post #68. It is true that synonimous mutations can sometimes have functional consequences, but that is not the general rule. Most synonimous mutations are neutral, and that's why you find them in conserved proteins, and when you compute the ka/ks ratio in a very conserved protein, its value is very low. 2) "the chytochrome b sequence have an absurd phylogeny that doesnt fit with evolution history. so does it mean that evolution isnt true in this case?" I have not studied that particular case, but I am sure that there are many molecules that contradict current models of evolutionary history. That can simply mean that current models of evolutionary history are wring under many aspects. I would not be surprised. Most "evolutionary histories" are built by assuming not only CD, but a lot of other things derived from the idea that unguided evolution is the origin of biological functional information. IOWs, they do not include design in their reasoning. I am certain that design is the principle behind all complex functional information in biology. Therefore, there is no surprise that theories which assume no design in biology reach wrong conclusions. But it's not the assumption of CD that is wrong, IMO. It's rather the assumption of unguided evolution.gpuccio
May 15, 2016
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Gpuccio
Now, how can a non coding sequence be designed? My favourite possible mechanisms, as already said, are: a) Guided mutations
And on that statement we are are in full agreement, this paper; http://www.ncbi.nlm.nih.gov/pubmed/22522932 has identified that there is evidence that mutations are not random, I particularly like the heading of the paper Evidence of non-random mutation rates suggests an evolutionary risk management strategy. Wallace was of course right and Darwin, clueless and if the mutation rates are not random its highly likely that the mutations themselves are guided as well.Andre
May 15, 2016
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Gpuccio: Of course new genes could be written also “from scratch” in the new species.
Those new genes won’t fit well with common descent (CD).
Gpuccio: Even in that case, CD can still be true for the rest of the genome (the genes which are shared between the ancestor and the final species), (…)
Of course. However the obvious problem is that CD is not true for new genes. CD as a context in which all sequences make sense fails — it simply cannot accommodate new sequences. And, mind you, the infusion of new sequences must have been MASSIVE since LUCA.
Gpuccio: Let’s say that you have some non coding sequence in primates, and that in humans, through a final mutation, it becomes an ORF (and therefore a protein coding gene) with a specific function for the protein. There are examples like that.
If I understand you correctly, the reasoning goes like this: the sequence was infused as non coding in an ancestor, so it doesn’t really count as infusion of new information and therefore we won’t have to reject the concept of CD. Please correct me if I'm wrong, but such attempts to push the problem back one step, seems to me like an elaborate attempt to square infusion of new information with CD.Origenes
May 15, 2016
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Eric Anderson: All that you say is very reasonable, and in no way it seems different to me from what I think. I will try to clarify better. "First, if new genes arise from non-coding sequences, are you suggesting that the nucleotide-to-amino acid sequence was already there and just became activated, or are you suggesting there was some kind of natural process whereby the coding sequence somehow came into proper formation (concatenation, accidental nucleotide changes, etc.)?" In the model I am proposing, and which already has some empirical support, what happens is exactly that at some point the nucleotide-to-amino acid sequence is already there, but is not translated because there are still a couple of adjustments missing, for example a start codon at the right place. IOWs, we have in some species a sequence of nucleotides which is non coding, probably not functional, but has the information potential to become an ORF if a couple of final "switches" are adjusted. In another species, which appears some time later, and which is "derived" from the ancestor species, that sequence appears as an ORF, is translated and generates a functional protein. Now, you ask: how could that sequence of nucleotide reach the information to become a functional protein coding gene, before it even could be translated? And the answer is: by design. A more or less gradual design prepares sequences in the non coding DNA so that in a future time they can become functional genes. This is a very strong model for design, if as I think it will become ever more supported by observations. Indeed, in such a model, NS cannot be invoked at all, because the sequence reaches its informational content before being even translated. Therefore, the right nucleotides must be in place before they can act through a symbolic correspondence to aminoacids through the genetic code. Therefore, to explain the functional information in the sequence, we have only two possibilities: 1) Design or 2) RV + sheer luck (Remember, NS cannot be invoked here). Guess which is the best explanation? :) Now, how can a non coding sequence be designed? My favourite possible mechanisms, as already said, are: a) Guided mutations b) Guided transposon activity Let's go now to the problem of how we get to be humans. I perfectly agree with you. Humans certainly have some new genes, but IMO they cannot explain the huge informational jump in human organization, especially at the brain level. The problem here is that we understand so little of those famous "procedures" which, through complex epigenetic regulations, guide cell developmnent and the organization of cells, tissues, organs and body plans. The information for those procedures certainly exists, and in some way it is transmitted from cell to cell, from being to being. But where and how is it written? I insist that such information: 1) Is certainly very complex. Neo darwinists love to believe that very complex functional arrangements, like a working nervous system of about 10^11 neurons and about 10^14 neuron connections, of which we understand almost nothing at present, can come out of a few simple mutations. I happily leave that kind of folly to them. I am certain that very complex procedures are necessary to organize such a result. 2) Is certainly written somewhere in the cell, in some way. Otherwise, how could it be transmitted from cell to cell and from being to being? So, I believe that humans have a huge amount of new and specific procedural information in their cells (in the genome, or epigenome, or anywhere else). I believe that we still don't understand where that information is written, and how, and therefore we cannot really understand what makes the difference between humans and chimps (or simply between any couple of different species).gpuccio
May 15, 2016
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VJT I concur with you analysis
So not only are 20% identical, but the 80% that are different are still so similar that much of the genetic basis for the phenotypic differences must be due to regulatory sequences and/or genes that have major effects.
If there is only an average of 4aa differences per protein that is about 64000 adaptions. (.8x 20000x4) Lynch's mathematical model runs out of adaptive resources at about 6 for neutral theory. ? I think the differences may be due to different splicing where exons are changed. It appears that phenotypic changes may be driven by splicing codes. The origin of these codes are unknown at this point. So if exons are shuffled the proteins may look similar but molded for different tissue types. Attached an article about splicing and its impact on evolution from MIT. Evolution: It’s all in how you splice it MIT biologists find that alternative splicing of RNA rewires signaling in different tissues and may often contribute to species differences. Anne Trafton, MIT News Office December 20, 2012 ?bill cole
May 14, 2016
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