Cornelius Hunter struggles to understand convergent evolution

I was hunting around for some blogging ideas recently when I came across this post by Wintery Knight. It’s basically a copy and paste job because Mr. Knight is not qualified to speak of anything in biology (and he has amply demonstrated as much). However, the person he extensively quotes, Cornelius Hunter, is also 100% unqualified to analyze the world of biology. I’ve written about Hunter in the past.

As in his last post that just barely merited a response on FTSOS, Hunter makes a series of confused remarks about convergent evolution. (For those who don’t know – such as Hunter – convergent evolution is the process by which species of usually distant relatedness will acquire the same trait independent of their last common ancestor.) Let’s take a look at how Hunter mangles this:

The theory of evolution states that the species arose spontaneously, one from another via a pattern of common descent. This means the species should form an evolutionary tree, where species that share a recent common ancestor, such as two frog species, are highly similar, and species that share a distant common ancestor, such as humans and squids, are very different. But the species do not form such an evolutionary tree pattern. In fact this expectation has been violated so many times it is difficult to keep track. These violations are not rare or occasional anomalies, they are the rule.

Hunter is only leading into his mention of convergence here, but he’s already off to an embarrassing start. He’s attempting to claim that we don’t see an expected pattern of descent because that pattern is premised on the idea that similar traits must come from closely related organisms. He is factually incorrect. All he has described here is one method for determining relatedness between species: morphology. And even then, he has grossly over-simplified the process. For instance, take the skull of a dingo versus the skull of a Tasmanian tiger. They resemble each other quite closely, but they aren’t exactly the same. The latter has two holes in the roof of its mouth, a characteristic of marsupials. Go further and one will see that they also have different genetic codings.

Many examples are the repeated designs found in what, according to evolution, must be very distant species. Such evolutionary convergence is biology’s version of lightning striking twice. To explain this evolutionists must say that random mutations just happened to hit upon the same detailed, intricate design at different times, in different parts of the world, in different ecological niches, and so forth.

Were Hunter to take a peak at the genes in a Euphorbia, he might notice that they are markedly different from the genes in a cactus. That’s because, while both plants are prickly desert survivors, one is from the Malpighiales order whereas the other is from the Caryophyllales order. They have significantly different genotypes, but similar phenotypes. In other words, Hunter’s argument that random mutations are always hitting “upon the same detailed, intricate designs at different times, in different parts of the world, in different ecological niches” is not only verbose, but entirely wrong. It would be as though he said home builders have hit upon the same intricate design because some use cellulose insulation while others use spray foam. It’s the same result by a different means.

Everyone has heard of the kangaroo and its pouch. It is a marsupial—mammals that give birth at a relatively early stage in development, and then carry their young in a pouch. There are a great variety of marsupials that are curiously similar to a cousin placental species. The flying squirrel (a placental) and the flying phalanger (a marsupial) are one such example. Because of their reproductive differences evolutionists must say they are distantly related on the evolutionary tree. Yet they have strikingly similar designs which must have been created independently by random mutations. Every mutation leading to the two different species must, according to evolution, have been random (that is, independent of any need). No, natural selection doesn’t help.

First, his mutation argument is still wrong. Second, it isn’t merely reproductive differences that tell us the flying squirrels (which are two independent groups of rodents) are different from the flying phalanger. There is also evidence from their genetic relatedness, not to mention the obvious fact that one is placental and the other a marsupial. Third, of course natural selection is relevant here. That’s the whole reason two species are able to converge on the same solution to similar problems; natural selection has found an efficient solution to one problem faced by two species.

Though evolutionists sometimes deny biological convergence, it is a scientific fact.

I don’t know what Hunter is talking about, but that’s okay because I don’t think he does either.

He goes on to quote from a recent paper:

In mammals, hearing is dependent on three canonical processing stages: (i) an eardrum collecting sound, (ii) a middle ear impedance converter, and (iii) a cochlear frequency analyzer. Here, we show that some insects, such as rainforest katydids, possess equivalent biophysical mechanisms for auditory processing…

Thus, two phylogenetically remote organisms, katydids and mammals, have evolved a series of convergent solutions to common biophysical problems, despite their reliance on very different morphological substrates.

Now, remember the crux of Hunter’s opening: Similar morphology is the same thing as intricate design, thus Jesus. Yet here we see a “reliance on very different morphological substrates”. That is, natural selection in some insects has hit upon the same broad method for attaining hearing as it has in mammals, but it goes about the process in a largely different way, relying upon the insect phenotype it has already given itself. So not only is Hunter’s argument wrong from the get-go, but even if we’re generous and grant him his incorrect basis, he still gets blown out of the water. He has managed to somehow be wrong in his wrongness.

It’s one thing when someone branches into biology from time to time, relying upon the insight of others. We see that with Wintery Knight (the reason being that he hasn’t a clue about the field). We can’t expect everyone to be an expert, even if they should know better. However, Cornelius Hunter is another story. This is a guy who fancies himself qualified and reasoned, able to break down complex scientific ideas. Yet what we see is a man unable to even come remotely close to getting much of anything right about a relatively simple idea. And he keeps trying, getting things wrong every. single. time.


The genius of Charles Darwin

By the time that an animal had reached, after numberless generations, the deepest recesses, disuse will on this view have more or less perfectly obliterated its eyes, and natural selection will often have affected other changes, such as an increase in the length of antennae or palpi, as compensation for blindness.

The above quote comes from On the Origin of Species. It is just one of the numerous instances where Charles Darwin, on the basis of his theory, makes a wonderful prediction that comes true so many years after the fact. In this case, his prediction has been shown to be true over and over; species which have gone millions of years in the dark lose their eyesight again and again. We see this especially in many species of cave fish, but it isn’t limited to the oceans:

With a leg span of only six centimetres and a body size of around twelve millimetres, the spider Sinopoda scurion is certainly not one of the largest representatives of the huntsman spiders, which include more than 1100 species. However, it is the first of its kind in the world without any eyes.

“I found the spider in a cave in Laos, around 100 kilometres away from the famous Xe Bang Fai cave,” reports Peter Jäger, head of the arachnology section at the Senckenberg Research Institute in Frankfurt. “We already knew of spiders of this genus from other caves, but they always had eyes and complete pigmentation. Sinopoda scurion is the first huntsman spider without eyes.”

One prediction the theory of evolution allows us to make today that Darwin couldn’t make in his lifetime is that the genes for vision in these now-blind species should exist but be broken. If they do not exist, then either there is some really funky timeline and divergence activity (that is, these are old lineages that evolved before their sighted brethren) and we should see a lot of other genetic differences or evolution just isn’t true. Neither one of those options is very likely, of course. What we observe instead is that, indeed, the genes for vision are a broken, jumbled mess. That isn’t the case yet for the above spider because, as far as I know, no such studies have been carried out, but it is the case wherever else these sort of species have had their genes analyzed.

One point I think that needs to be made sure with Darwin’s quote here is this: Natural selection is unlikely to be the only factor in the disappearance of eyes among these species*. In fact, it could have little to nothing to do with the process at all. Vision in the dark is a useless thing, so natural selection may obliterate it for the sake of saving energy or preventing potential injury to a sensitive body part, but I believe it is much more likely that it simply did nothing. It neither selected for nor against vision. As a result of the lack of positive selection, mutation and genetic drift took over and vision in these species simply faded away.

*I really have two points here. First is the one I just made in the above paragraph. Second is the fact that Darwin was referencing natural selection in regard to it creating some compensation for blindness, not in regard to it directionally causing the blindness.

Not once

Where are all the pre-Cambrian primates anyway?

Chromosome 2

It has been proposed and well evidenced that human chromosome 2 is the result of a fusion event between two chromosomes in our evolutionary past. Briefly, here is the evidence:

All great apes except humans have 24 pairs of chromosomes. We only have 23. That means we need an explanation for such a difference that dates back only a relatively short period of time (5-7 million years). As it happens, human chromosome 2 shows strong evidence of being two fused chromosomes. The way we know this is that all chromosomes have telomeres and centromeres. Telomeres are repeating units of DNA that serve to protect the ends (and therefore middles) of chromosomes, sort of like a good pair of shoes and a strong helmet. Centromeres are DNA units located somewhere between the telomeres of chromosomes, generally relatively close to the center. Their function is to help assemble the two parts of a chromosome during cellular replication and reproduction. In human chromosome 2, we see that there are actually two telomeres fused together in the center. There are also telomeres on the end, but between each end and the center are centromeres. That means we have three telomeres (one of which is fused) and two centromeres.

I bring this up because I was recently reading yet another excellent post by The A-Unicornist and he was dealing with this stuff:

ID is really nothing but an argument from ignorance – it claims that certain things simply cannot be explained by science, so it must be ‘best explained’ by a designer instead. Take for example this post from The New Creationist. I often point creationists to the Ken Miller video where he explains the Chromosome-2 fusion in humans, because it’s a perfect example of the theory of evolution making a falsifiable prediction that ended up being powerful evidence that evolution is true – something that ID has never done and in principle cannot do, which is why it will never be a science. Now, this “new creationist”, who incidentally sounds just as credulous as the old ones, argues that such a fusion is impossible – that the chromosome should never have been able to fuse at all.

Being that I’m not a biologist, I have no idea how to directly refute what he’s arguing. But it’s conspicuously odd that rather than, I dunno, ask a biologist or two (like, golly I dunno, write a letter to Ken Miller?), he simply frames his argument as though the unanswered question itself creates a major problem for the theory of evolution.

Since I’ve used chromosome 2 as an argument for evolution, I am familiar with the creationist responses. As such, I want to address what the blogger known as The New Creationist is arguing:

If the fused chromosomes in an end-to-end fusion are ripped apart by the centromeres during cell division and cells must divide to produce an embryo then how does an embryo develop with two previously fused but now ripped apart chromosomes? We know that the loss of just one chromosome would be lethal and here we have the loss of both of the two
fused chromosomes. If fused chromosomes do not make it through cell division then how could a fused chromosomal configuration be a result of common descent since there would be no descendants by a biological pathway. Such would be miraculous. Indeed, I believe it is a miracle not only because it can not be explained by any natural pathway but also because it is contradicted by experimental data.

What he is trying to say (and what he later says a little more clearly) is that two centromeres would cause division and assembly to occur in two separate places. This would be an all around mess that would prevent not only mitosis, but meiosis as well. So what could the solution be? Well, he answers it himself:

Now, it has been proposed that the deactivation of one of the centromeres in the fused chromosome would prevent the rupture and subsequent loss of the newly formed fusion…

And that is the case. One of the centromeres has been deactivated. One possible reason for this could relate to the fact that the area near the deteriorated centromere (the pericentromeric sequences) has gone through a large number of duplication events, but this isn’t known and requires certain confirming evidence around other deactivated centromeres. I don’t know if any significant research has been done in this area since the 2006 paper about chromosome 2.

The New Creationist continues:

…but this poses another equally lethal problem during the pairing off of homologous chromosomes.

Let’s say that if C2A fused with C2B forming C2 (which has 2 centromeres) in the paternal germ line, the male’s sperm. Now, that sperm would have to fertilize an egg where both C2A and C2B not having been fused would have to pair off with the paternal C2 BUT if C2 has been prevented from being ripped apart because one of its centromeres has been deactivation then the corresponding maternal C2B (or C2A) will not combine with C2 in the mother’s egg because that centromere would have been deactivated.

In other words, he is saying that if two ancestral primates had offspring with the fused chromosome, then that offspring would have 23 chromosomes whereas the rest of the population still had 24. Mating between the two could not occur as a result, thus the fused chromosome could never make it beyond a single generation.

The most obvious solution to this problem is that several members of a population experienced a fusion event. It could have been a completely chance event, or it could have been due to a particular mutation that had spread down the line. That is, my money is on a mutation existing in a population that caused the fusion between two specific chromosomes. Perhaps all the pericentromeric duplications (which pre-date the fusion event, incidentally) gave rise to a gene that was free to mutate neutrally in the population. After some time, it managed to survive the generations, and made a marked difference. (That’s what has happened, minus the specific duplication events, with Richard Lenski’s E. coli.) Or maybe a mutation popped up just out of completely random chance, as opposed to being connected to any particular type of event. It’s hard to say just how any of this happened, but there are good hypotheses to be had on the question.

To conclude, the first argument presented here was defeated before it was even made. One of the two centromeres was deactivated long ago, as stated in the original paper. Indeed, that very paper even suggested a correlating factor in centromere deactivation that could be useful for future research. As for the second argument, I’m going to give Mike the last word:

[T]he fact that an explanation is either unknown or not immediately apparent would not refute the fact that the theory of evolution made this falsifiable prediction, nor would it suggest that there cannot be a rational explanation at all. Our new creationist seems to think that because he does not know how to explain it that a rational explanation is not merely unknown, but in principle impossible. Ergo, Goddidit. That ain’t how science works, kids.

Evolution, fruit flies, and counting

Don’t let any creationist tell you complex things don’t come from simple precursors:

US and Canadian researchers have evolved a population of fruitflies that can count. The result, presented on 9 July at the First Joint Congress on Evolutionary Biology in Ottawa, Canada, supports the notion that the neural mechanisms underlying basic arithmetic skills first emerged hundreds of millions of years ago. It could also eventually offer a key to understanding why some people have problems with numbers…

During a 20-minute training period, flies were exposed to either two, three or four flashes of light — two and four flashes coincided with a vigorous shake administered by placing a electric toothbrush next to the box containing the flies. After a brief rest, the flies were returned to box and shown the light flashes. Despite a dislike for being shaken, most of the flies were not able to learn to associate the negative stimulus with the number of flashes. But 40 generations later, they could.

The researchers caution that the work is preliminary and that they do yet know what genetic changes are behind the insects’ evolved number sense.

What I find interesting is exactly how this constitutes selection pressure. The flies certainly don’t like being shaken, but that’s entirely irrelevant if there isn’t some sort of reproductive advantage to be had from recognizing when the shaking will occur. Clearly there is, and we could speculate all day long as to why flies that associate the flashes with negative stimulus pass on more of their genes than the other flies, but I would like to see some experimental data showing the details. Does shaking disorient the flies? Does it interrupt the mating process? Does it affect fertility? Perhaps the paper that comes from all this can shed some light.

Now excuse me while I go murder the fruit flies that appear to have evolved to make my kitchen just awful for the past week.

Butchering science

This is just a mess.

I have written in the past about Jack Hudson’s tendency to butcher science. There are a lot of examples of him doing this, but one of the most egregious was when he concluded that because fruit fly populations under laboratory conditions come to allelic fixation at a different rate and/or way than asexual populations, that must mean there is some flaw in evolutionary theory. (In re-reading his post, I’m also seeing that he concluded something else equally egregious: He said that mutations which affect mRNA structure as opposed to protein sequence is evidence that random mutations cannot lead to new traits.) In short, it is highly evident that Jack read a popularized article about a recent study, glommed a few lines from the original research, and then went about drawing inept conclusions.

And now he’s back at it.

Let me give an actual summary of this most recent study first:

Stickleback fish are found all around the world. They exist in a number of streams, rivers, lakes, and oceans due to their great ability to adapt quite quickly to their environment. This opens up a great opportunity to take a look at their genes to see just what regions are evolving.

Now, what often happens in these sort of studies is that researchers will choose selected areas or candidate genes and compare them. It’s a tried and true method, but it probably isn’t the whole picture. While researchers can grow various species (usually of bacteria), objectively know how they’ve diverged and evolved under laboratory conditions, and then compare what they know to phenotypic changes brought on by alterations in protein-coding genes, there has been a push for a long time to sequence more and more full genomes. One result has been information overload (even when the full genome of something has not been sequenced; the technology that allows full genome sequencing also inherently allows easier partial sequencing), but that’s not a bad problem to have. So for this study, the biologists sequenced 21 three-spined stickleback genomes. Their goal was to determine the underlying molecular basis for adaptive evolution in the fish: Do they evolve by way of regulatory or coding changes?

What the team found was that 147 regions vary in freshwater versus marine stickleback populations. Of these 147 regions, 17% were linked to coding genes, 41% to regulatory regions, and 42% could not be classified cleanly (though, as the neat little graph under “Proportion of regulatory and coding change” in the paper says, they are probably regulatory).

So the big conclusion is this. Stickleback evolution is dominated by regulatory changes – changes involving areas which control genes. (Coding changes are still important, but this study indicates a possible shift in focus as it becomes cheaper and easier to sequence whole genomes.) The regions prevalent in stickleback evolution are relatively few; we keep seeing the same areas get tweaked over and over, leading to independent (and often convergent) solutions for the same sort of environments.

Now let’s look at Jack’s butchery:

But these findings are actually quite contrary to the sort of evolution often advocated by Darwinian evolutionists. Instead of incidental mutations coding sequences leading to the production of new proteins (and conceivably, novel structures and systems) the researchers found that the changes were primarily to the same sets of regulatory sequences in separate populations of sticklebacks…

While the researchers continue to use the term ‘evolutionary change’, the reality is this is nothing like the sort of change described by the modern evolutionary synthesis, a theory which relies on natural selection acting on genetic mutation.

To summarize this inanity: Jack is saying that evolution predicts that changes in species should occur almost exclusively by way of natural selection working on random mutation. He’s wrong. What evolution says is that change will occur by a number of mechanisms – random drift, hitchhiking via linkage, bottlenecking, horizontal gene transfer, and others. Random mutations culled by non-random selection will result in changes, certainly. And that’s what we see quite frequently in the laboratory and nearly 1/5 of the time in this stickleback study. However, the presence of other mechanisms is not somehow counter to evolutionary theory. Indeed, I think embryologists would be rather upset to learn that their field undermines evolution since the regulation of development – not necessarily or even usually by coding regions – has a huge impact on the way species change over time.

Yet I haven’t even gotten to the kicker:

The very fact that the researcher describes these as “key genes that control evolutionary change” contradicts the ordinary notion of evolution itself, which is purportedly an unguided process.

This reminds me Mary Midgley’s complete misunderstanding of Richard Dawkins’ The Selfish Gene. Midgley complained, chiefly, that Dawkins’ use of “selfish” was wrong because genes don’t have emotions. It was risible and I don’t know as Dawkins should have bothered responding. Naturally, I have to wonder if I should bother with the likes of Jack Hudson.

The language being employed by the scientists behind the stickleback study does not indicate that there is any guiding mechanism to evolution. They obviously are not claiming that regulatory genes direct evolution in a predetermined way. All they are saying is that these genes are a major factor in evolutionary change. It would be as if I said that my gene for lactase controls my tolerance for lactose (dairy products, more or less). That does not mean there is a little man sitting on a section of my DNA, tinkering away because he desires that I ingest milk.

Sorry to keep this going, but there are a lot of kickers in this one:

If natural selection acting on incidental mutations were actually capable of producing the radically different body plans, structures and systems we find throughout the plant and animal kingdoms, then we wouldn’t expect to see the consistent similarity of genetic modifications that we do with regard to the various populations of sticklebacks.

It would be generous to say this is a strain on logic. It absolutely does not follow that the predominance of regulatory genes excludes the importance of random mutation. Moreover, this study is not looking at millions of years, so extrapolation out that far should be constrained.

The changes wouldn’t be a matter of merely regulating extant genes, but the origination of new genetic capabilities.

Jack is, in essence, claiming that regulatory changes do not count as evolution. Unfortunately for him, we have thousands of different species of sticklebacks that attest to significant change over time – and now we know they’ve been doing it with a lot of help from their regulatory genes. So even if there was something to Jack’s claim on its own, it wholly crumbles when we hold it up to all the different stickleback populations around the globe.

Genetic sequencing continues to demonstrate that there are limits to biological variation.

This is in reference to specific creationist-proposed limitations, something not supported by an iota of this study. That is, this claim boils down to Jack saying that because sticklebacks evolve in a large number of ways by virtue of relatively few regulatory regions, species are constrained to microevolutionary changes. Again, this is a logic fail. The presence of changes by way of natural selection operating on regulatory genes does not exclude changes by way of natural selection operating on random mutation. Anyone who bothered to honestly look at this study would know that. (17% and perhaps more of the regions map to actual genes, for Christ’s sake.)

As I’ve said a few times before, what takes a creationist 30 seconds to say takes an educated person hours to untangle. And just as with my last post about butchered science, this didn’t take quite that long, but the sentiment remains true.