I mentioned before that IDEA clubs insist that expertise is optional; well, it’s clear that that is definitely true. Casey Luskin, the IDEA club coordinator and president, has written an utterly awful article “rebutting” part of Ken Miller’s testimony in the Dover trial. It is embarrassingly bad, a piece of dreck written by a lawyer that demonstrates that he knows nothing at all about genetics, evolution, biology, or basic logic. I’ll explain a few of his misconceptions about genetics, errors in the reproductive consequences of individuals with Robertsonian fusions, and how he has completely misrepresented the significance of the ape:human chromosome comparisons.

In Miller’s testimony, he talked about a basic fact of biology: most apes have 24 pairs chromosomes for a total of 48, while we have 23, for a total of 46. We are familiar with the fact that errors in chromosome number, called aneuploidies, within the human species are devastating and have dramatic effects; the most familiar aneuploidy is Down syndrome, but there are others, which all lead to very short lifespans and extremely disabling phenotypes. Most aneuploidies are embryonically lethal and lead to spontaneous abortions. If evolution is valid, we should be able to see how that occurred historically, in a way that requires no mysterious interventions and only natural, observable mechanisms. Miller summarized it quite well.

Now, there’s no possibility that that common ancestry which would have had 48 chromosomes because the other three species have 48, there’s no possibility the chromosome could have just got lost or thrown away. Chromosome has so much genetic information on it that the loss of a whole chromosome would probably be fatal. So that’s not a hypothesis.

Therefore, evolution makes a testable prediction, and that is, somewhere in the human genome we’ve got to be able to find a human chromosome that actually shows the point at which two of these common ancestors were pasted together. We ought to be able to find a piece of Scotch tape holding together two chromosomes so that our 24 pairs — one of them was pasted together to form just 23. And if we can’t find that, then the hypothesis of common ancestry is wrong and evolution is mistaken.

The answer is, of course, that the evolutionary prediction holds true: we do find the homologs of two genes fused together in our chromosome 2. We have the human and chimpanzee sequences, and we can see the same genes in our chromosome 2 that are found on two other chimpanzee chromosomes; we can see the structure of two centromeres in our one chromosome, and also the relics of telomeres (normally at the ends of chromosomes) imbedded in the middle. It is an open-and-shut case.

Casey Luskin doesn’t understand any of it. His response is to throw out a series of foolish speculations that have long since been discarded and that completely contradict all of the evidence.

Why couldn’t it be the case that the common ancestor had 23 distinct chromosomes, and one chromosome underwent duplication in the line that led to apes? Or maybe the common ancestor had 20 distinct chromosomes and there have been 4 duplications events in the ape line, and 3 in the human line?; or maybe the ancestor had 30 distinct chromosomes and there have been 6 fusion events for ape-line but 7 fusion events for the human-line.

Do you see my point? Simple chromosome-counting or comparisons of numbers of chromosomes does not lead common ancestry to make any hard predictions about how many chromosomes our alleged ape-human common ancestor had. So, under Miller’s logic, there is no reason why a chromosomal fusion event is a necessary prediction of common ancestry for all upper primates.

That’s pathetic. The reason evolutionists proposed a chromosomal fusion event is that all of the duplication events he proposes would have major phenotypic consequences (Down syndrome is caused by a duplication of one very small chromosome, for instance) and would represent a serious obstacle to evolution—Miller stated so very plainly. Some lineages are tolerant of that kind of massive genomic change, but ours is not. Multiple independent fusions are possible, but improbable; we can see evidence of it in species that have diverged for a long time (mouse and human chromosomes are dramatically rearranged relative to one another, for instance), but apes haven’t been separated as long. We have also had evidence for about 40 years that on a gross level, the structure of the chromosomes in all apes was very similar.

Luskin is tossing around these wild ideas in a very lawyerly tactic—he’s trying to cast doubt on the best explanation by pretending there are a multitude of alternatives. Those alternatives are not reasonable, and he knows it: he even admits it.

So I am more than willing to acknowledge and affirm that Miller did provide some very good direct empirical evidence for a chromosomal fusion event which created human chromosome #2. But I’m more interested in two other questions: if we accept Miller’s chromosomal fusion evidence as accurate, then (1) is his chromosome fusion story good evidence for Neo-Darwinian common ancestry between humans and apes? Or (2) does it perhaps pose great problems for a Neo-Darwinian account?

The answer to question (1) is “NO” and the answer to question (2) is “YES!”

Oh, dear. This is where Luskin goes off the rails, and abandons all reason.

(1) is a bogus framing of the issue. The fusion is not evidence of common ancestry; it’s the common genomic content of all ape chromosomes that is the evidence. The fusion accounts for a superficial difference in the appearance of the karyotype, but the underlying genetic sequence is what exposes the relatedness of humans and other apes. Luskin harps on this bizarre notion of his, that the occurrence of a fusion is the key to human evolution.

All Miller has done is documented direct empirical evidence of a chromosomal fusion event in humans. But evidence for a chromosomal fusion event is not evidence for when that event took place, nor is it evidence for the ancestry prior to that event.

Yes, that is correct. Miller wasn’t claiming anything about when it occurred, or that the fusion says anything about prior ancestry: it’s the sequence, stupid. But look here, here’s Luskin’s real agenda.

Given that we had a 48-chromosome ancestor, we don’t know if our 48-chromosome ancestor was an ape or not. For all we know, our 48-chromosome ancestor was a part of a separately designed species, as fully human as anyone you meet on the street today. There is no good reason to think that going from a 46-chromosome individual to a 48-chromosome individual would make our species more ape-like.

Separate creation. We ain’t descended from no monkeys. Miller’s point is that chromosome number is not a good indicator of different ancestry, but Luskin wants to turn that around and claim any ol’ ancestry is therefore equally valid…but it’s not. It’s the sequence, not the fusion, that tells us of our relatedness. And of course no one has proposed that a simple chromosome fusion or separation is responsible for the differences between us and other apes.

That humans are most closely related to apes and that we all had a common ancestor in the relatively recent past is not a point in contention by any reasonable scientist. This is the kind of false malarkey the IDists want to push in our schools—it’s simply bad science to deny common ancestry.

What about Luskin’s point (2), that the fused chromosome is a problem for the neo-Darwinian account? It’s more nonsense (what else would you expect?).

Under Neo-Darwinism, genetic mutation events (including chromosomal aberrations) are generally assumed to be random and unguided. Miller’s Cold-Fusion tale becomes more suspicious when one starts to ask harder questions like “how could a natural, unguided chromosomal fusion event get fixed into a population, much less how could it result in viable offspring?” Miller’s account must overcome two potential obstacles:

(1) In most of our experience, individuals with the randomly-fused chromosome can be normal, but it is very likely that their offspring will ultimately have a genetic disease. A classic example of such is a cause of Down syndrome.

Not quite. What we see in humans is a classic instance of a Robertsonian translocation. These happen quite often—1 in 900 births bear a fusion of this kind—and they cause no immediate problems at all. The affected individual has a full and normal genetic complement; it’s just that two of their chromosomes are stuck together. It can cause reduced fertility, but is unlikely (except in some known, specific cases) to lead to offspring with a genetic disease.

Let me explain why. Assume we have a set of genes (a) found on one chromosome, and a set of genes (b) found on another. Everyone has two copies of each set, so in a normal diploid cell, we have (a) (a) (b) (b). In meiosis, the cellular mechanisms segregate the chromosomes in an orderly way, so each gamete gets one set (a) and one set (b), each gamete looks like this: (a) (b).

In an individual with a Robertsonian fusion, though, each diploid cell looks like this: (a) (b) (a:b). They have three chromosomes instead of four, even if they do have the proper doses of (a) and (b). Now when meiosis occurs, the cell has to sort 3 chromosomes into two cells, and there are multiple ways this can happen:

(a) (b)	a normal gamete : normal
(a:b)	a gamete carrying the fusion, but with the normal complement of genes: normal
(a) (a:b)	a gamete with an extra (a)—lethal
(a)	a gamete with an no (b)—lethal
(b) (a:b)	a gamete with an extra (b)—lethal
(b)	a gamete with a no (a)—lethal

As you can see, several of the combinations produce viable gametes, and this individual can have healthy children with no detectable problems, although half of them will carry the Robertsonian fusion. The other gametes have serious problems, and will typically lead to very early miscarriages, especially if they involve a large chromosome, like chromosome 2. They will have more problems conceiving, but their children will be normal.

If the fusion chromosome spreads through the population, something interesting will happen, and some people will have diploid cells like this: (a:b) (a:b). All of their gametes will be (a:b), and all will be normal. Fusions like this put up measurable but not at all insurmountable barriers to reproduction and can make it easier for carriers to reproduce with each other, so they can be mechanisms for reproductive isolation and speciation.

Again, Luskin doesn’t understand this basic concept, and he compounds his error with quote mining and poor scholarship.

(2) One way around the problem in (1) is to find a mate that also had an identical chromosomal fusion event. But Valentine and Erwin imply that such events would be highly unlikely: “[T]he chance of two identical rare mutant individuals arising in sufficient propinquity to produce offspring seems too small to consider as a significant evolutionary event.”

(Erwin, D..H., and Valentine, J.W. “‘Hopeful monsters,’ transposons, and the Metazoan radiation”, Proc. Natl. Acad. Sci USA, 81:5482-5483, Sept 1984)

The problem in (1) is not a problem. As I just explained, you don’t need a mate with an identical fusion event to successfully reproduce.

His choice of an article to back up his assertion is weird. The article is from 1984, for one thing; why dig up a 22 year old article to support a basic point? For another, the article does not discuss the viability of hybrids with Robertsonian fusions at all. It is specifically about the possibility of large scale mutations that generate major morphological novelties.

The article is a short speculative work that suggests a way to get around the objection they mention, and that is the center of Luskin’s argument—in other words, it’s a paper that says how Luskin is wrong. (It also happens to be a proposal I don’t find too likely: Erwin and Valentine suggest that one way the frequency of novel mutations could rapidly rise to overcome the problem is by site-specific horizontal transfer of transposable elements. Mmmm, maybe, but I’d want to see more evidence of such transformations associated with key innovations.)

Fortunately for the short attention span of creationist, their quote is from the second sentence of the paper. I can only assume they didn’t bother to read any further. Does anyone else have this mental image of Discovery Institute “scholars” poring over science papers with almost no comprehension, but happily plucking out random sentences here and there that they can misuse? I suspect they have a compendium of such fragments that their fellows use, without the need of ever having to actually read any science.

In other words, Miller has to explain why a random chromosomal fusion event which, in our experience ultimately results in offspring with genetic diseases, didn’t result in a genetic disease and was thus advantageous enough to get fixed into the entire population of our ancestors. Given the lack of empirical evidence that random chromosomal fusion events are not disadvantageous, perhaps the presence of a chromosomal fusion event is not good evidence for a Neo-Darwinian history for humans.

No, no. Duplications in humans lead to genetic diseases. Miller was explaining that there is a normal genetic mechanism for fusions that represents an evolutionary pathway without the detriment of a major duplication/deletion that leads to our current chromosome arrangements.

The only guy proposing a path by way of duplications and their concomitant problems was Luskin.

Miller may have found good empirical evidence for a chromosomal fusion event. But all of our experience with mammalian genetics tells us that such a chromosomal aberration should have resulted in a non-viable mutant, or non-viable offspring. Thus, Neo-Darwinism has a hard time explaining why such a random fusion event was somehow advantageous.

Whoa, irony meter, calm down. Luskin telling us about “all of our experience with mammalian genetics”? He’s wrong. He doesn’t even have basic textbook knowledge of genetics. Our experience with mammalian genetics tells us that he is babbling out of his butt: fusions have no such problem yielding viable offspring.

If you bother to take a look at the list of articles maintained by the IDEA center, you’ll see that the majority of them are by Luskin, and he’s usually pontificating about similarly imaginary problems in evolutionary theory, problems that are actually with his own shameful lack of knowledge about the subject. This pathetic ignoramus is the primary source of information for the collegians they’re trying to recruit into their IDEA clubs? I’d consider it a source of embarrassment to have an organization dedicated to such foolishness on my campus.