Saturday, 22 September 2007

Re-Cell Cycling Front-loading Pt. II

Remember Dover? For those of you who don't, it was the latest stand by creationists to get creationism into schools (under the guise of "intelligent design"). At the centre of the case was a text designed for schools called Of Pandas and People. During Michael Behe's testimony, he was presented with a quote from the new version of the text, which is still in preparation:
Sudden emergence holds that various forms of life began with their distinctive feature already intact, fish with fins and scales, birds with feathers and wings, animals with fur and mammary glands.
I bring this up because I want to continue where I left off fisking this paper

Sherman, M. (2007). Universal genome in the origin of metazoa. Cell Cycle 6: 1873-1877. Link

Previously, I went through the evidence Sherman put forward to suggest that there was a problem for evolutionary biology, and humbly suggested that it may not be as much as a problem as he thought, and that if he was to make sweeping statements, he might like to support them. So, now let's get on to what he suggests explains the problems he sees. In a nutshell, it is sudden emergence with huge brassy shiny knobs on.

This is what he writes:
Here I propose a hypothesis that answers the questions posed above, and offers experimentally testable predictions. This hypothesis postulates that (1) shortly (in geological terms) before Cambrian period a Universal Genome that encodes all major developmental programs essential for every phylum of Metazoa emerged in a unicellular or a primitive multicellular organism; (2) The Metazoan phyla, all having similar genomes, are nonetheless so distinct because they utilize specific combinations of developmental programs. In other words, in spite of a high similarity of the genomes in phyla X and Y, an organism belonging to phylum X expresses a specifc set of active developmental programs, while an organism belonging to a different phylum Y has a distinct set of "working" programs specifc for phyla Y.
(as in my previous post, all grammatical mistakes are in the original. I don't want to indicate them all, so let's just give Sherman a sic note)

In other words, every species had every gene, but not all of them are used. Now, to experienced watchers of ID on the blogosphere, this is a familiar notion, John A. Davison's Prescribed Evolutionary Hypothesis. Davison is a crackpot, but let us not judge Sherman on those grounds. Certainly, Sherman has thought through his ideas more, and is probably a sane, normal person.

So, Sherman's idea is that a Universal Genome appeared in the Cambrian, causing an explosion. Since then, the process of evolution has just been one of changes in the switches in pre-existing developmental programmes. Sherman implies that these changes are not genetic (as all organisms started with the same Universal Genome), so it's not awfully clear how he thinks developmental changes have occurred. Perhaps he should throw some epigenetics into the mix.

So, how did the Universal Genome appear? Ah, Sherman says nothing. It's taken as a given that supporters of ID will say that it can't say anything about the identity of the designer, but this is going one step further - stuff just appeared without mentioning the possibility of a designer. You see, it's Sudden Emergence, only without the mammaries.

Sherman quickly seeks to address what he sees as a fundamental problem: if the universal genome was in all Metazoa initially, why don't we see it in all now? The solution is obvious - genes have been lost over time:
A beautiful illustration of such a loss is a Wnt gene family. In humans, there are nineteen Wnt genes belonging to twelve families. In Hydra. on the other there are two Wnt genes that correspond to two families found in humans. Simple analysis of this finding within the framework of the classical model suggests that additional human genes have developed from ancestral Wnt genes found in Hydra. However, Anemona that belongs to a distinct branch of Cnidaria has eleven Wnt genes belonging to eleven families found in humans. Therefore, it is quite obvious that many Wnt gene families, possibly the entire set, exists in the gene pool of the primilive Metazoan phylum, and various members of Wnt families were lost in different species within this phylum.
Waste not, Wnt not.
Accordingly, the proposed model predicts that in various groups of Cnidaria we will find many diverse gene families that function in more advanced phyla.
Or that they have also become lost.

Sherman expands on his ideas:
The "Universal Genome" hypothesis does not contradict any well-established data on the genetic evolution (e.g., gene duplications or accumulation of mutations, molecular clock. etc). but suggests that genetic evolution could shape and improve function of developmental programs.
It's a pity Sherman missed out all that well know data about large chunks of DNA suddenly appearing in a genome, without any immediate function. I'm a bit sceptical about his suggestion that the hypothesis doesn't contradict data on the accumulation of mutations, so let's see how he defends that:
Yep, that's how he does it. Once more, make a bold statement, don't give any argument or evidence to support it and move on. For the moment, so shall we.

Sherman fills in a couple of details (including a bit of special pleading for genes have only been lost is some lineages - there must be a special mechanism for their conservation in others. Again, just a a statement, not backed up), and then gets on to the "this is really science" part:
There are two main testable predictions of the presented hypothesis, which are absolutely critical for validation of the model; (1) full or parts of the developmental programs characteristic to higher taxons must be encoded in genomes of lower taxons, and (2) blocks of genetic information encoding these developmental programs in more primitive taxons must be useless in these taxons.
What happened to waste not Wnt not? Sherman is saying that primitive organisms must still carry genetic code for more advanced developmental programmes. But he's already accepted that they can lose genes. So, (1) can't be critical. (2) is more interesting - one would need to show that the genetic information was present, but not expressed in the "primitive" taxa. Sherman, of course, doesn't suggest this. Instead, he tells us that the common ancestor of Arthropoda and Chordata didn't have eyes (as we have already seen, this is not quite right), but yet jellyfish have eyes, and they are controlled by similar genes to those in Drosophila. Oh, and as part of this argument, he points out that jellyfish don't have a central processing unit like a brain, so it is unclear how they could process and integrate what they see. Once again, because we are ignorant of something, it can't possibly happen.

Sherman also suggests that we could try and induce development of these more advanced programmes, for example by over-expressing Pax6 in the sea urchin, and seeing whether it develops eyes (and becomes a see urchin, I suppose). It's not clear to me why over-expression would make a difference: we already know that it is expressed in the sea urchin's foot. Without, apparently, an eye being developed. Could it be that other genes involved in eye production are missing? The public needs to know!

We also get another prediction:
Another indication that latent developmental program is present in a lower taxon would be expression of such a program in higher taxons derived from the lower one in a seemingly convergent processes. For example a possible experiment would be to activate development of circulation systems of mammalian or bird types in lizards or even in Xenopus [a frog]. The circulation systems in mammals and birds appear to be very similar, however, they developed from the reptilian system independently in these taxons. Therefore it seems likely that Reptilia possess the program of development of the circulation system of the mammalian/bird type and requires only a minor switch to activate it.
This sounds like we would end up with a reptile that was developmentally very confused. Note we're told that Reptilia have the programme for development, but we're not shown any evidence. Where are the homologs and orthologs for the genes? Is Sherman unable to BLAST the Xenopus genome to see if the genes are there? (in case you're wondering, I'm too lazy to chase this up myself).

Sherman suggests his second prediction could be tested by deleting genes and seeing if there is a physiological effect, e.g. the genes for the adaptive immune system in the sea urchin. This makes sense (although you might have to attack the sea urchin with a pathogen afterwards, to see if it responds). Except that it's not clear what one would conclude if nothing happened - Sherman has already discussed the possibility that genes are lost, so he could claim that that's what has happened in this case. In other words, the predictions don't provide potential falsification (although if they were found to be correct, they would provide a powerful verification of the idea).

So, we have a paper that makes some dodgy claims from ignorance that evolution can't explain the Cambrian explosion or the evolution of body plans, followed by and alternative hypothesis which explains nothing that can't be explained by evolutionary biology, relying on gaps in our knowledge to create doubt. And it says nothing about the elephant in the room - how sudden emergence happened. The key part of the hypothesis - how developmental information appeared - is just stated and then left aside.

The whole premise of Intelligent Design as science was that one could investigate design without asking about the designer (because, obviously, that would mean admitting you thought the designer was the god of Abraham). Sherman has taken this to the next stage - he doesn't even mention the possibility of a designer.

I mentioned in my first post that I was suspicious about this paper. That was because the grammar looked odd (the mistakes were in simple grammar, but complex structures were correct). That was before I read this, from the Disco Institute (p20) (pdf):
On the other hand, reading the papers on evolution published in respectedscience journals like Proceedings of the National Academy of Science or Nature, one is surprised at the weakness of the arguments. Indeed, the standards of proof in the field are much lower than in the rest of biology. Such papers would never make it through the peer-review process if they concerned molecular or cellular biology. Of course, there are obvious reasons for such low standards, including the difficulty of testing evolutionary hypotheses through experimentation. But if the theory is based on poor arguments, why have criticisms of it not succeeded in convincing mainstream scientists?
Poor arguments? Ha ha ha ha! Now, this guy must be spoofing us, and the DI.

As for the jourmal, it is asking to be spoofed. This is part of the journal's explanation of why one should publish there:

  • Rapid response to presubmission
    inquiries (usually within the hour). Most papers are rejected without
    external review. (papers send for external peer-review are expected to
    be published). During presubmission inquiry, reviewers will be
    contacted to accelerate further review. Authors are encouraged to
    suggest and decline potential reviewers.

  • Ultra-rapid peer-review (usually within one-two days)

  • Papers
    rejected from other top journals (e.g., Nature, Science, Cell), if the
    authors choose, may be submitted with previous reviews and decision
    letters. This allows for the consideration of a paper without sending
    for additional review.

So, the journal takes an hour to decide if a paper is good enough - if it's sent out to review, then it will have to be pretty crap to be rejected. And there is pressure on the referees to comment on a manuscript very quickly. This must have a negative impact on the quality of the refereeing - sometimes you have to go through a paper carefully, and spend time checking references, and also thinking about it - often I need time to work out why I'm not sure about a paper, or to work out what to recommend. The final bulletpoint says to me that the journal is desparate - they want good papers (doesn't every journal?), so they are prepared to cut corners to do so.

The journal is desparate to do things quickly, so it looks like if you wanted to get a dodgy or hoax paper published, this is a good journal to do it with. I hope that is what happened. Otherwise Michael Y. Sherman will have to justify why he can submit a paper in whcih he ignores basic norms of writing science - you know, backing up your argument with evidence. And whether this is a hoax or not, Cell Cycle has to justify how it can publish paper which nobody there has even read properly.

EDIT: Forgot to hat-tip Albatrossity for the pdf. Thanks!

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