The Institute for Creation Research reveal their scientific illiteracy.
In a recent blog posting (No Fruit Fly Evolution Even after 600 Generations), Institute for Creation Research ‘science’ writer Brian Thomas misinterprets (deliberately or otherwise) two classic experiments in genetics, and one that has been recently published. The ICR website doesn’t permit commenting, presumably to exclude people popping over to point out errors in their writing.
The first example concerns work conducted by Nobel prizewinners Christiane Nusslein-Volhard and Eric Wieschaus, and published in several peer-reviewed papers in the 1980s (see for example Nature 287, 795-801 (30 October 1980) | doi:10.1038/287795a0). The reason why Nusslein-Volhard and Wieschaus (along with Ed Lewis) won the Nobel Prize for Physiology or Medicine (there is no Nobel Prize for Biology) in 1995 was that they identified many of (if not most of) the genes that underpin the specification of body plan in the embryonic and adult development of the fruit fly Drosophila. The significance, of course, being the high level of conservation between these Drosophila genes and their counterparts in other animals, including humans. Of course the ICR don’t like this, since it correlates pretty well with evolutionary theory.
Now, what is it that Thomas thinks is the key take-home work from the ground-breaking experiments of Nusslein-Volhard and Weischaus?
If evolutionary biologists could document such evolution in action, they could vindicate their worldview and cite real research to support their surreal claims. In 1980, this search for proof led researchers to painstakingly and purposefully mutate each core gene involved in fruit fly development. The now classic work, for which the authors won the Nobel Prize in 1995, was published in Nature. The experiments proved that the mutation of any of these core developmental genes―mutations that would be essential for the fruit fly to evolve into any other creature―merely resulted in dead or deformed fruit flies. This therefore showed that fruit flies could not evolve.
This paragraph illustrates Thomas’ lack of understanding. Nusslein-Volhard and Weischaus clever stratagem was to realise that many of the genes that are required for correct embryonic development would be recessive lethal mutations, because loss of function would result in severely abnormal development. Nusslein-Volhard and Weischaus therefore generated collections of Drosophila strains bearing lethal mutations that cause death in the embryonic stages. They then examined embryos from each of these strains for embryos with evidence of abnormal development. Typical examples would include abnormal segmentation, embryos with incorrect specification of anterior and posterior and so forth.
So a real examination of Thomas‘ claims do not hold water: Nusslein-Volhard and Weischaus did not “painstakingly and purposefully mutate each core gene involved in fruit fly development”, they generated a large number of mutants and looked for those that specifically affected embryonic development. Also Thomas’ claim that the mutants “merely resulted in dead or deformed fruit flies” is also wrong: the whole point of the experiment was to identify mutations that yield abnormal embryos. Indeed the experiments were not aimed at demonstrating that fruit flies could evolve. On the other hand, the similarity between the Drosophila genes that Nusslein-Volhard and Weischaus identified and the counterparts found in all segmented animals provides very good support for the evolution of all these taxa.
On the subject of Richard Lenski’s E. coli experiments, I refer Brian Thomas to P. Z. Myers’ Pharyngula blog, which discussed the paper (Historical contingency in the evolution of E. coli), and dealt with the creationist misunderstanding (wilful or otherwise): creationists across the internet have spent a good deal of time trying to discredit Lenski’s work and failing.
Thomas also reveals his poor grasp of biology in his discussion of a recent paper in Nature (Burke et al (2010) Genome-wide analysis of a long-term evolution experiment with Drosophila. Nature 467, 587–590 doi:10.1038/nature09352), which describes a lengthy experiment in which a population of Drosophila was selected for rapid development over about 600 generations. Normal Drosophila can develop from egg to adult in about 10 days at 25oC: this experiment yielded flies that developed about 20% faster. As an experimental biologist (rather than an armchair creationist) might expect, a number of correlated phenotypes also evolved, including shorter lifespan, smaller body size and reduced starvation resistance.
To simplify the findings of the paper, detailed and extensive DNA sequencing revealed that in comparison between selected and unselected populations:
One sequence variant every 175 bases
Over 37000 of these variants potentially impact on gene function
662 variants in 506 genes are predicted to have a significant effect on function
The majority of the genes are known or predicted to play a roles in development
I wonder whether the ICR don’t have a subscription to Nature or that they are unwilling to pay for the pdf – it certainly seems as though Thomas’ reading is limited to the abstract. Thomas’ conclusion from his ‘reading’ of the paper is:
The study’s authors wrote, “In our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed.”
They suggested that perhaps there has not been enough time for the relevant mutations to have become fixed. They also suggested an alternative—that natural selection could be acting on already existing variations. But this is not evolution, and it is actually what creation studies have been demonstrating for many years.
The abstract, which is freely available on the Nature website, reads (in part):
[...] in our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed. More parsimonious explanations include ‘incomplete’ sweep models, in which mutations have not had enough time to fix, and ‘soft’ sweep models, in which selection acts on pre-existing, common genetic variants. We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.
Actually, may take on this paper (and bear in mind that this population genetics is not my field in Drosophila genetics) is that it has demonstrated the genetic consequences of long term artificial selection for a characteristic which probably leads to pretty disadvantageous outcomes for the animal (reduced lifespan, reduced body weight, reduced starvation resistance), and the point the authors make is that the dynamics of genetic diversity under selection is rather more complex than seen is simpler, asexually reproducing organisms. None of this is particularly contentious, and it in no way represents evidence against evolution.
Except in the eyes of the ICR and its staff writers.
H/T: Psiloiordinary (BCSE)