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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
Wait a minute. ... only 340 beneficial mutations explain the difference? I am not buying that. I am basing that on the Sexual reproductive systems alone. Try as I might to conceive of the posssiblity, it falls flat and again it's because the Sexual reproductive systems, even those of our last common ancestor would have been too precise to allow what people are assuming. If I had a single example of a crockoduck I would be convinced.Andre
May 14, 2016
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Hi Bill Cole, Thank you for your post, citing an article by Glazko, G., V. Veeramachaneni, M. Nei, and W. Maka?owski, "Eighty percent of proteins are different between humans and chimpanzees" (Gene 346 (2005 Feb 14): 215-9). I googled its title and came across a commentary on the article at the pro-evolution Website: http://www.evolutionarymodel.com/chimphumanproteins.htm The commentary makes a couple of important points:
The publication does not say that "80% of our [proteins] do not exist in apes;" rather it says that 80% don't have identical sequences of amino acids (big difference)... But the question that some creationists hope you won't ask is how much different did they find those 80% of proteins to be? Answer: unexpectedly little... [The commentary includes a table showing the percentage of proteins showing 100%, 99%, and 98% sequence identity between humans and chimps for different functional categories. It appears that many chimpanzee proteins are at least 98% similar to human proteins - VJT.] 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.
I hope that helps.vjtorley
May 14, 2016
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Hi Eric Anderson, Thank you for your post. You ask:
Maybe what you are saying is that the claim of an unbroken chain of reproduction from an ape-like ancestor can help explain the similarities between chimps and humans, and at the same time we need an outside infusion of information to explain the significant characteristics that make us human?
Yes. That is indeed my position. May I add that 22.4 million neutral mutations are believed to have taken place in the human line since it diverged from the line leading to chimps. These would on my account be entirely natural changes, and they represent 99.999% of the mutations that were fixed in the human line. The 340 beneficial mutations that are believed to have taken place in the human line during the same period represent only a tiny fraction (0.001%) of the mutations that were fixed in the human line, but it is these mutations that explain the important physical differences between humans and chimps. As I envisage it, many (but not all) of these mutations would have been intelligently directed. I would also wholeheartedly concur with gpuccio's comments in #68 and #69 above.vjtorley
May 14, 2016
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Hi mk, Thank you for your posts. You suggest that the orangutan is closer to human beings than the chimp is, morphologically, citing this article in support of your claim: http://news.nationalgeographic.com/news/2009/06/090623-humans-chimps-related.html However, the article you cite dates back to 2009. More recent research with a much larger dataset of morphological characters indicates that the chimpanzee is the species most similar to human beings, morphologically speaking: http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2699.2010.02354.x/full http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2699.2012.02759.x/fullvjtorley
May 14, 2016
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VJT Eric Gpuccio THIS IS THE REAL ISSUE: http://www.ncbi.nlm.nih.gov/pubmed/15716009# Abstract The chimpanzee is our closest living relative. The morphological differences between the two species are so large that there is no problem in distinguishing between them. However, the nucleotide difference between the two species is surprisingly small. The early genome comparison by DNA hybridization techniques suggested a nucleotide difference of 1-2%. Recently, direct nucleotide sequencing confirmed this estimate. These findings generated the common belief that the human is extremely close to the chimpanzee at the genetic level. However, if one looks at proteins, which are mainly responsible for phenotypic differences, the picture is quite different, and about 80% of proteins are different between the two species. Still, the number of proteins responsible for the phenotypic differences may be smaller since not all genes are directly responsible for phenotypic characters.bill cole
May 14, 2016
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hi gpuccio. you said: " OK, there can certainly be some functional adjustments from species to species, and part of the diversity can be functional, but all of it? I really don’t think so."- first. 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. 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?mk
May 14, 2016
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gpuccio @65: Let me start off by saying that I know you have looked into this issue in more detail than I and, coupled with the fact that I have a great deal of respect for your opinion, my inclination is to defer to you on this issue. If I may, however, perhaps I can articulate just a couple of points of intellectual unease. 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.)? Second, and more importantly, I think we all recognize that the traditional evolutionary story of random changes to DNA nucleotide sequences won't cut it when it comes to turning an ape-like creature into a human. The idea that some new genes might suddenly arise is interesting, to be sure. But it is only one step removed from the old Darwinian storyline and, importantly, doesn't address all the other required aspects. Having a new gene-coding sequence pop into my DNA is indeed impressive, but it won't get me anywhere on the path to functionality. Specifically, I still need to have mechanisms that decide when to activate that gene, how much to produce, where to chaperone it to, how it will be used in the cell, and on and on. Furthermore, many (perhaps most) gene-products are primarily used in concert with others in larger complexes (one of the things Behe has been exploring the past decade). As a thought experiment, let's make the conservative assumption that at least one difference between humans and chimps requires a molecular machine as complex as a bacterial flagellum. Even if all the 40+ proteins popped into the DNA all at once, there is still an incredible amount of coordination, orchestration, planning, timing, and so on that are required before the morphological result can be realized (and before the molecular machine can be visible to natural selection). Just as horizontal gene transfer, co-option, and similar theories don't help much to explain the origin of new organisms, the idea of new genes arising within an organism, from non-coding regions or otherwise, suffers a similar limitation. ----- I agree there are some interesting data points in all of this and that we are just scratching the surface. I respect the viewpoint of those, including Behe, who argue for "common descent." I try to pin down exactly what they mean, because based on the evidence I have seen to date, I remain highly skeptical that anything close to a purely natural process can be responsible for turning an ape-like creature into a human. Might there be some continuity across generations and even across species? Perhaps. But the need for design to get from A to Z is clear.Eric Anderson
May 14, 2016
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Eric Anderson: "Maybe what you are saying is that the claim of an unbroken chain of reproduction from an ape-like ancestor can help explain the similarities between chimps and humans, and at the same time we need an outside infusion of information to explain the significant characteristics that make us human?" I definitely agree with this statement. I would add the the claim of an unbroken chain of reproduction from an ape-like ancestor can help explain not only the similarities between chimps and humans (or any other couple of related species), but also the differences due to neutral variation. It is absolutely true that we need an outside infusion of information (explicit design) to explain the significant characteristics that make us human (or that make any species what it is).gpuccio
May 14, 2016
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To all: OK, here is a very simple example of what I mean by differences in similar proteins as evidence of common descent. Let's take myoglobin, a globin with a definite function. Let's look at it in vertebrates. The human protein is 154 AAs long. Here are the results of blast with 4 vertebrates which can be reasonably considered at increasing chronological proximity with humans in natural history. I am not assuming any refined tree here, just the simple fact that bony fish and birds and mammals and primates are in some gross sequence if compared to humans. Humans are primates, and primates are mammals. Both bony fish and birds are vertebrates but not mammals, and it is perfectly reasonable that bony fish are more ancient than birds. Now, let's look at the blast results: Best hit in bony fish: Sarda chiliensis: bitscore 131; expect 5.00E-38; identities 71 (48%); positives 90 (60%); length 147; Best hit in birds: Acanthisitta chloris bitscore 248; expect 2.00E-82; identities 118 (77%); positives 135 (87%); length 154; Mouse: bitscore 264; expect 1.00E-89; identities 129 (84%); positives 141 (91%); length 154; Chimpanzee: bitscore 310; expect 3.00E-110; identities 153 (99%); positives 153 (99%); length 154; OK, I think that's enough. The problem is, how can you explain the relative diversisty between fish myoglobin and human myoglobin (only 48% identity), and the gradual increasing similarity to the human form, up to the almost identity in chimpanzee? One could say that all those differences are due to functional restraint, but that is really unlikely: after all, the protein remains rather similar for structure and function. OK, there can certainly be some functional adjustments from species to species, and part of the diversity can be functional, but all of it? I really don't think so. The best explanation is: the split between fish and mammals is older, and the protein we find in fish and the protein we find in humans have been subject to neutral variation for more than 400 million years. The functionally constrained part of the sequence has remained similar (which explains the strong 48% identity), but what could change has changed, in such a long divergence time. Compare that with the 84% identity with the mouse protein. The split between rodents and the ancestors of primates is probably about 80 million years ago. And, obviously, chimpanzee has a protein which is almost the same as humans. 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. For clarity, I must say that I remain convinced that part of the observed diversity can be explained functionally, and can be designed. But definitely not all of it.gpuccio
May 14, 2016
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vjtorley @60:
What I mean by [common descent] is that humans and chimps share a common ancestor. That’s all.
Share a common ancestor in the sense that they both descended from the common ancestor through a natural process of generation-to-generation reproduction and random chance changes accumulating over time? That would be the normal understanding of common descent. I agree with you that there must have been some outside infusion of information and, I would argue, not just a nucleotide tweak here or there, but some really fundamental complex specified changes. That is where the shorthand term "common descent" starts to break down, because presumably we would then mean that humans descended from some ape-like creature by the normal pathways of common descent, plus new information-directed design.
But where your analogy breaks down is that computers don’t have babies, and primates do.
Certainly no analogy is perfect, but it still raises an important concept. What is it that you image having babies brings to the table? What is it about having babies that can turn an ape-like creature into a human? Unless we are falling back on the tired evolutionary assertion that copying errors, mutations, random changes creeping in during reproduction, and the like can produce new functionally-integrated, information-rich organisms, then there is nothing special about ape-like creatures having babies that helps turn them into a human. Bear with me a moment while I try to better understand your position: Maybe what you are saying is that the claim of an unbroken chain of reproduction from an ape-like ancestor can help explain the similarities between chimps and humans, and at the same time we need an outside infusion of information to explain the significant characteristics that make us human?Eric Anderson
May 14, 2016
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hi guys. the vitellogenin protein have other function then making yolk. so even if it was functional in the human past it cant be evidence for a commondescent. the mice-rat different is also very easy to explain. we know for example that chimp is closer to human then orngutan from genetic prespective. but actually the orangutan is the closer to human from morphological prespective: http://news.nationalgeographic.com/news/2009/06/090623-humans-chimps-related.html so closer genetic similarity doesnt mean a close morphology. ther is a different between variation and function.mk
May 14, 2016
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Origenes: "This interpretation of common ancestry appeals to me and it makes perfect sense to say that, those retained sequences you speak of, have ancestors. However, by the same logic, newly introduced sequences do not have ancestors — they are orphans. How does one square such unrooted new information with common ancestry?" New genes arise in species. They are obviously designed. We still don't know much on their origin, but it seems that at least in a number of cases they can arise from non coding DNA sequences. That is a very good argument for design and for CD at the same time. 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. Now, is a sequence in an ancestor species has already much of the potential for the future protein coding gene, but still it is non coding, no kind of gradual RV + NS can be invoked: a sequence which is non coding cannot be selected for the functions of a protein which is still non existent. So, if the sequence of the non coding DNA gradually acquires the correct configuration to be able to code for a functional protein, and then, in a new species (for example humans) it is finally "released" as a protein coding gene by the final addition of a start codon, only design can explain that process. At the same time, CD between the ancestor and the final species must be true too, so that the sequence can be prepared in the ancestor and activated in the final species. New genes can also arise by transposon activity. Many genes have that kind of signature. Many times I have argued that transposons are perfect potential tools for protein engineering by a biological designer. Of course new genes could be written also "from scratch" in the new species. 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), while new genes can simply be added during the engineering process. In general, I prefer the scenario where new genes derive from existing non coding sequences, either by simple directed mutations or by transposon activity. There is already some evidence for that kind of process. For a recent paper about de novo genes, you can look at this: http://rstb.royalsocietypublishing.org/content/370/1678/20140332gpuccio
May 14, 2016
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VJT Here is the other paper I discussed with Michael Behe. Evolutionary dynamics of coding and non-coding transcriptomes. Necsulea A1, Kaessmann H2. Author information Abstract Gene expression changes may underlie much of phenotypic evolution. The development of high-throughput RNA sequencing protocols has opened the door to unprecedented large-scale and cross-species transcriptome comparisons by allowing accurate and sensitive assessments of transcript sequences and expression levels. Here, we review the initial wave of the new generation of comparative transcriptomic studies in mammals and vertebrate outgroup species in the context of earlier work. Together with various large-scale genomic and epigenomic data, these studies have unveiled commonalities and differences in the dynamics of gene expression evolution for various types of coding and non-coding genes across mammalian lineages, organs, developmental stages, chromosomes and sexes. They have also provided intriguing new clues to the regulatory basis and phenotypic implications of evolutionary gene expression changes.bill cole
May 14, 2016
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VJT ,Thank you for your comments here. I truly appreciate them.
Exactly how does this falsify the hypothesis of common descent?
The alternative splicing differences makes new proteins which can account for the dramatic phenotypic differences. This shows a large biochemical divergence between man and chimps. Way beyond the differences between rats and mice. When you compare DNA sequences you are unconsciously spinning because that is just part of the story. I agree that if you define common decent as the change from one specie to another via a directed mechanism then we are in sync, but honestly I think that claiming knowledge of the design mechanism is wild speculation at this point. As Michael Behe said in our conversation the "how" of the design is beyond our current understanding at this point and he avoids these conversations.bill cole
May 14, 2016
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VJTorley, thank you for your response.
Torley: I understand “common descent” as a hypothesis about organisms, not as a hypothesis about genes or complex structures.
It seems to me that common descent is foremost a hypothesis about how new species are introduced by the designer of life. According to this hypothesis, new species do not go directly from the designer's lab to earth, but are instead introduced by being born out of somewhat similar species. An example of this is "the process whereby humans arose from a chimp-like ancestor". How does one picture such an event? Am I correct to say that, according to this version of the common descent hypothesis, there were once at least two unfortunate human beings with chimp-like parents?Origenes
May 14, 2016
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Hello, a FAQ has been added to my original article that includes a response to Michael Behe's contribution to this conversation. I hope this helps address your questions. In particular, thank you Bill Cole for raising this to Michael Behe's attention. http://swami.wustl.edu/evidence-for-evolutionProf. S. Joshua Swamidass
May 14, 2016
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Hi Eric Anderson, You write:
When 99% of evolutionary scientists use or hear “common descent” it is understood to mean — assumed to mean — something that occurred by purely undirected natural and material processes.
That's not how I mean the term "common descent." What I mean by the term is that humans and chimps share a common ancestor. That's all. You write that common descent without a proposed mechanism is “very fuzzy.” It is vague, in the sense that it does not specify the source of new information. That vagueness is intentional: it's a hypothesis about material causes, rather than efficient causes. You also write:
We might, for example, look at something like the Intel Pentium II processor and the Pentium III processor and note a lot of similarities, including a nice, obvious temporal development over time. We could rationally say that there is a “descent” relationship from II to III. But the key — where the rubber meets the road — is that there was an additional infusion of information, additional architectural parameters, additional functional integrated specified complexity that allowed II to “descend” and turn into III. In other words the Pentium III processor came about by design, not by “common descent,” at least not as that term is generally understood.
I entirely agree with your point about the infusion of information, and I believe this is what happened in the human line. But where your analogy breaks down is that computers don't have babies, and primates do.vjtorley
May 14, 2016
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Hi everyone, As I see it, common descent is a hypothesis about material causes, not efficient causes. What it tells us is that whatever process gave rise to us and the information in our genome, the material which that process worked on and modified was the genome of an apelike creature. Simple as that.vjtorley
May 14, 2016
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Hi Bill Cole, I've just had a look at the paper, The Evolutionary Landscape of Alternative Splicing in Vertebrate Species by Nuno L. Barbosa-Morais et al. (Science Vol. 338, 21 December 2012), which you cited above in support of your claim that gene timing and alternative splicing data contradicts common descent. A few excerpts:
AS [Alternative splicing] detection is approximately twice as frequent in all analyzed primate organs as in the equivalent organs from mouse and other species (Fig. 1A and fig. S1). Moreover, there is an overall decline in AS frequency as the evolutionary distance from primates increases. These differences are significant (P < 10^?10, Mann-Whitney U tests), are robust to different methods of AS frequency detection, and are independent of the variability in AS detection rates between individuals within the same species (Fig. 1A and fig. S1). Genes with the highest AS complexity in human are significantly enriched in cytoskeleton-associated functions (P < 0.03) (table S1), which suggests that AS-directed diversification of the cytoskeleton may have been a driving force in the evolution of increased cellular complexity in vertebrate species... We next investigated the relative rates at which AS and GE [gene expression] have evolved. From pairwise comparisons of PSI values in homologous tissues, we observe an overall increase of PSI divergence from human with evolutionary time (Fig. 2A)... However, the overlap between sets of splicing code features used in a given pair of species decreases with increased evolutionary distance (Fig. 3C and fig. S12; see also below)... However, because our results also indicate that vertebrate splicing codes diverged with increasing evolutionary distance, and because specific subsets of AS events could not be reliably predicted using the splicing code, changes in trans-acting factors likely also contributed to evolutionary differences in AS.
Exactly how does this falsify the hypothesis of common descent? You also write:
What does it mean to share a common ancestor? Do you mean that there was a split 6 million years ago and we came about through natural variation. If this is true how would you account for all the novel proteins, epigenetic timing differences and the different alternative splicing sequences. How would you account for the 2500 AA difference in the length of the titan protein?
No, I don't think we came about through natural variation. Where did I ever say that? I'm quite happy to acknowledge that novel human proteins were engineered. All I'm saying is that the Engineer modified the genes of an apelike creature in order to produce us.vjtorley
May 14, 2016
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bill cole @55:
We need a very clear definition of common decent. This idea is very fuzzy without RMNS as a mechanism.
Good point. When 99% of evolutionary scientists use or hear "common descent" it is understood to mean -- assumed to mean -- something that occurred by purely undirected natural and material processes. If someone is proposing "common descent" that does not occur by purely undirected natural and material processes, then fine. But they need to be clear about what they are proposing. As I understand gpuccio, for example, he proposes that there are infusions of information at various stages along the way -- meaning, design interventions in the history of life -- while there is some continuity of descent preserved. Fair enough. But, as you say, common descent without a proposed mechanism is "very fuzzy." We might, for example, look at something like the Intel Pentium II processor and the Pentium III processor and note a lot of similarities, including a nice, obvious temporal development over time. We could rationally say that there is a "descent" relationship from II to III. But the key -- where the rubber meets the road -- is that there was an additional infusion of information, additional architectural parameters, additional functional integrated specified complexity that allowed II to "descend" and turn into III. In other words the Pentium III processor came about by design, not by "common descent," at least not as that term is generally understood.Eric Anderson
May 14, 2016
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VJ
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.
I think your conclusion here is because you do not understand the complete biochemical picture, based on available evidence today. I believe that Cornelius does. IF YOU LOOK AT THE GENE TIMING AND SPLICING DATA YOU WILL SEE DIRECT CONTRADICTION OF YOUR CONCLUSION. MAKING YOUR CONCLUSION FROM DNA COMPARISON ALONE NOT COMPETENT SCIENCE.bill cole
May 14, 2016
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VJ
Second, I’d like to point out that common descent is simply a hypothesis about ancestry. It does not say anything about the processes whereby we diverged from our ancestors. If Dr. Hunter wishes to point to unique designs found in various lineages, then he is welcome to do so. But that’s an argument for Intelligent Design, not an argument against common ancestry.
We need a very clear definition of common decent. This idea is very fuzzy without RMNS as a mechanism.bill cole
May 14, 2016
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Andre, I suspect that artists paint our hominin ancestors with whites in their eyes (sclera) in order to make them look more intelligent (and more human-like) than they actually were.vjtorley
May 14, 2016
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Andre, I believe that the ancestral species in the line leading to modern humans were designed by the Creator. That includes Homo ergaster. At least some of the beneficial mutations which led to this species were engineered. New information was thus inserted into the ancestral human genome by the Creator.vjtorley
May 14, 2016
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Hi Origenes, Thank you for your comments. You write:
I don’t understand how unique designs are “not an argument against common ancestry”, because, by definition “unique designs” do not have an ancestral design. If common descent is to be taken as a context in which all sequences, designs and information make sense, then ‘orphan’ sequences, designs and information should not exist.
I understand "common descent" as a hypothesis about organisms, not as a hypothesis about genes or complex structures. I do not think that all of the complex structures found in the human body are necessarily modifications of structures found in other animals. And I do not think or all of the genes in our DNA are necessarily modifications of genes found in other animals. I find it quite plausible that the Designer (whom I believe to be God) created some new genes and some new structures in the human lineage, although I'm a lot more certain about us possessing new structures than I am about us possessing new genes. Most of the so-called "orphan genes" described in the literature are nothing of the sort, since they have 98% similar counterparts in chimps, as I discovered last year: https://uncommondescent.com/intelligent-design/double-debunking-glenn-williamson-on-human-chimp-dna-similarity-and-genes-unique-to-human-beings/ However, I'm quite sure that the human brain, which is the most complicated machine known to exist in the universe, was designed.vjtorley
May 14, 2016
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Andre: "So are we then in full agreement that CD is first and foremost an assumption?" I think we can agree, if I specify better the meaning of words in my epistemological views about science. In brief, I believe that all empirical sciences are made of inferences about observed facts. We can call them hypotheses or theories, but inferences they are anyway. Only darwinists are so crazy to think that inferences can magically become facts. So, Common Descent is IMO an inference which can in some measure explain some oberved facts, and I have also tried to explain briefly what those facts mainly are (if I have time enough, I shall post something more detailed about that). Inferences can be good or bad, but they are never definitely true. All scientific inferences, even the best, can in principle be falsified by new facts. An inference is good when it explain rather well observed facts, and when at presnt there is no better inference to explain those facts. IMO, CD is at present the best explanation for those fcats I have mentioned, but no one is obliged to think so. In my view of science, no scientific theory, even the best, must necessarily be accepted by all scientists. There are physicists who don't agree with the Big Bang theory, or even with quantum mechaniscs (Einstein was an example). They have their arguments, and they could be right. But at present, I would say that the Big Bang and quantum mechanics remain by far best explanations for many things. Science is not about final truths. It is about theories. Each person can and must decide for himself what theories he accepts as best. In that sense, constructive skepticism (IOWs, the faculty of motivated doubt) is a precious resource in science. Unfortunately, as you well understand, today the word skepticism has come to mean biased dogmatism (its logical opposite). But constructive doubt is a very good thing. But what do we mean with the word "assumption"? My answer is rather simple. Let's take the example of CD. For me, CD is a reasonable inference, not as strong as ID, but rather good. Others can obviously disagree. Now, when we want to make new inferences, we often take some previous inferences and consider them as established (at least tentatively), so that we may base new reaosning and inferences on those premises. That is an "assumption". For example, I assume CD when I make inferences about the functional information in proteins by their conservation through species. I have argued many times that the alpha and beta chains of ATP synthase are wonderful examples of functionally constrained sequences, and thereofer of design. Why? Because they are strongly conserved from bacteria and archaea to humans. The reasoning assumes CD and neutral variation, and very simply says: if these sequences have remained strongly similar throughout about 3.5 billion years of CD, during which they have been exposed, like any other sequence, to neutral variation, the only possible explanation is that they cannot change more than that, because changes are eliminated by negative selection. Therefore, they have a very high content of functional information (in the order of thousands of bits), and the oonly possible explanation of their existence is design. This whole reasoning has no meaning if I don't assume CD and neutral variation. Again, I have tried to explain my views as clearly as possible.gpuccio
May 14, 2016
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Mung: As you can easily see, I have not commented on what Swamidass says, because I am not really interested in arguments about how religious people should see this or that. I see little of scientific relevance is such discussions. Frankly, I am also not interested in olive branchs of any kind or in relational adjustments. I am only interested in science. ID theory is tha best explanation for biological information, period. The only olive branch I can conceive of is an admission of that simple fact. My only interest here was to clarify some aspects about the Common Descent issue, which as you can see remains a very "hot" issue for ID people. That I have tried to do.gpuccio
May 14, 2016
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Gpuccio: You see, I look at the problem [common ancestry] not so much from the point of view of species, but rather from the point of view of information and sequences. The important point is that sequences “travel” through different species retaining a physical continuity.
This interpretation of common ancestry appeals to me and it makes perfect sense to say that, those retained sequences you speak of, have ancestors. However, by the same logic, newly introduced sequences do not have ancestors — they are orphans. How does one square such unrooted new information with common ancestry? VJTorley doesn’t see it as a problem:
If Dr. Hunter wishes to point to unique designs found in various lineages, then he is welcome to do so. But that’s an argument for Intelligent Design, not an argument against common ancestry.
I don’t understand how unique designs are “not an argument against common ancestry”, because, by definition “unique designs” do not have an ancestral design. If common descent is to be taken as a context in which all sequences, designs and information make sense, then ‘orphan’ sequences, designs and information should not exist.Origenes
May 14, 2016
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Dr Torley What is meant by when Homo Ergaster arose? Is this via the process of gene duplication, aka copy errors?Andre
May 13, 2016
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Gpuccio I just want to highlight that my use of the word skeptical must please not be conflated with the materialist version of intellectual dishonesty. Like I said I am not opposed to CD, I am not convinced by it. Our material friends use of skeptical is not the same.Andre
May 13, 2016
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