I've been spending quite a bit of time debunking ID (Intelligent Design) arguments on various other blogs. This blog is for storing some of my longer arguments. I prefer to call ID 'Imagination Deficit' as I feel that better describes it.

Tuesday, July 04, 2006

Just So

One things that the attackers of science (including ID advocates) frequently do is accuse scientists of constructing 'just-so stories'.

This is first of all a deeply ironic claim, given that the ID advocates either are unable to or refuse to identify any candidate for a designer. Therefore the ID 'explanation' for - well - everything is: 'an unknown intelligent designer did it using unknown methods for unspecified reasons at an unknown time'.

The above doesn't even reach the lofty heights of a 'just-so story' because there is absolutely no detail whatsoever. At least Kipling supplied some detail with his stories, even if it was entirely fanciful!

So, let's contrast this contentless, meaningless ID 'explanation' with some examples of the kinds of evolutionary narratives that the ID advocates claim are 'just-so stories', and see if we can spot any differences.

I'm going to use gene duplication as my example. I'm not going to reference any scientific journals whatsoever in this section.

'Just-so story'

A scientist while investigating a bacterial genome discovered that two genes doing apparently different tasks were almost identical in sequence, only differing by a few base pairs. This was a very interesting discovery, and the scientist decided to investigate a bit further. The first thing he did was to sit down and think about ways in which this related genes could have been produced. He came up with a few explanations, but the one he thought was the most likely was that the original gene had been copied (duplicated) in it's entirety, and then one of the copies had been changed by point mutations until was performing a different task to the original.

(The above explanation is typically labelled a 'just-so story' by ID advocates. We have some evidence. The scientist has constructed a explanation to account for it. There is no other evidence at this point that the explanation is correct. Science typically refers to these kinds of explanations as 'hypotheses', and they are acknowledged to be entirely tentative in nature.)

Having come up with a perfectly reasonable explanation for the origin of these two very similar genes what does the scientists do next? Does he drop the subject having explained it to his satisfaction and then move on to his next project? Actually he doesn't. He decides that this hypothesis needs testing to see if it actually correct. So the scientist has a think about what predictions he can make from his hypothesis, and how he can therefore design some tests for it.

If this gene duplication has occurred once, the scientist thinks it is likely that similar duplications could have occurred elsewhere in the genome. So finding other related pairs of genes ('homologs') would be additional evidence to strengthen the explanation. There may be multiple duplication events to create a 'family' of related genes, which would provide more evidence. There is a chance that having had a duplication event, one of the copies could lose it's start sequence and become 'redundant', finding these would also provide extra evidence. And of course the best evidence of all would be to have an organism with a fully sequenced genome and to have a duplication event actually happen, so when the genome is examined again later there are now two (or more) copies of a gene where before there was one.

(So the whole point of the scientific hypothesis above is that can be used to create testable predictions. This is why it is not a 'just-so story'. It's a starting place for further investigation. The hypothesis might turn out to be wrong or incomplete.)

The scientist then widens his search and looks for other closely related pairs of genes. And he finds them. And so do other scientists in other organisms. He looks for families of related genes. He finds those too. And so do other scientists. He looks for redundant genes ('pseudogenes'). And finds them. As do other scientists. Other scientists using his research as a basis observe the duplication event occuring. The gene duplication hypothesis moves from being a tentative hypothesis to being a known evolutionary mechanism with multiple strands of overlapping evidence that are fully consistent with each other.

Other scientists use the now known and familiar concept of redundant pseudogenes to form their own hypotheses. One group start with the observation that most mammals have a gene for producing vitamin C and chimps and humans do not have this gene. This group of scientists use the two known (and repeatably tested and confirmed) phenomena of common descent and redundant pseudogenes to predict that the ancestor of chimps and humans once had a functional vitamin C gene and that it has become a redundant pseudogene. They also predict that that the human and chimp redundant pseudogenes will be more closely related to each other (less small point mutations) than the chimps will be with various other ape species. They look for the redundant vitamin C pseudogene in humans and chimps. And they find them. And sequence analysis shows the close relationship exactly as predicted.

So from the first original predictive testable hypothesis we have spawned a whole raft of new experiments, repeatedly tested and confirmed the predictions of the hypothesis and used the new mechanism to drive the next round of scientific hypotheses. Just so.

The real science

Of course at the moment the above is just my condensed version of the kind of events that led to the discovery of gene duplication and redundant pseudogenes. No scientific narrative is ever complete without references to the real science.

A pubmed search on the term "gene duplication" gives more than 3000 references, some of them are below.

Gene families include the hemoglobin/myoglobin family, the immunoglobulin superfamily, the family of seven-membrane-spanning domain proteins, the G-protein family, the serine protease family and the homeobox family.

Observation of gene duplication:

Brown, C. J., K. M. Todd and R. F. Rosenzweig, 1998. Multiple duplications of yeast hexose transport genes in response to selection in a glucose-limited environment. Molecular Biology and Evolution 15(8): 931-942.

Evolution of duplicate genes:

Hughes, A. L. and R. Friedman, 2003. Parallel evolution by gene duplication in the genomes of two unicellular fungi. Genome Research 13(5): 794-799.

Lynch, M. and J. S. Conery, 2000. The evolutionary fate and consequences of duplicate genes. Science 290: 1151-1155. See also Pennisi, E., 2000. Twinned genes live life in the fast lane. Science 290: 1065-1066.

Ohta, T., 2003. Evolution by gene duplication revisited: differentiation of regulatory elements versus proteins. Genetica 118(2-3): 209-216.

Park, I.-S., C.-H. Lin and C. T. Walsh, 1996. Gain of D-alanyl-D-lactate or D-lactyl-D-alanine synthetase activities in three active-site mutants of the Escherichia coli D-alanyl-D-alanine ligase B. Biochemistry 35: 10464-10471.

Zhang, J., Y.-P. Zhang and H. F. Rosenberg, 2002. Adaptive evolution of a duplicated pancreatic ribonuclease gene in a leaf-eating monkey. Nature Genetics 30: 411-415. See also: Univ. of Michigan, 2002, How gene duplication helps in adapting to changing environments.

The 'missing' vitamin C gene:

Nishikimi, M., R. Fukuyama, et al. (1994) "Cloning and chromosomal mapping of the human nonfunctional gene for L-gulono-gamma-lactone oxidase, the enzyme for L-ascorbic acid biosynthesis missing in man." Journal of Biological Chemistry 269: 13685-13688.

Ohta, Y. and Nishikimi, M. (1999) "Random nucleotide substitutions in primate nonfunctional gene for L-gulano-gamma-lactone oxidiase, the missing enzyme in L-ascorbind acid biosynthesis." Biochimica et Biophysica Acta 1472: 408-411.

Some more examples of human redundant pseudogenes:

Rouquier, S., A. Blancher, et al. (2000) "The olfactory receptor gene repertoire in primates and mouse: Evidence for reduction of the functional fraction in primates." PNAS 97: 2870-2874.

Haag, F., Koch-Nolte, F. et al. (1994) "Premature stop codons inactivate the RT6 genes of the human and chimpanzee species." Journal of Molecular Biology 243: 537-546.

In conclusion

So the ID claim that evolutionary narratives are 'just-so stories' is patently, demonstrably false. Evolutionary narratives when they are first hypothesised are acknowledged to be tentative and a mere starting point for further investigation. Once the real science has been done, evolutionary narratives themselves can 'evolve' from tentative hypotheses to become tested, known and fully accepted mechanims of evolution. These mechanisms can then be used as the basis for further tentative hypotheses, in the confidence that the mechanisms themselves are well known and repeatedly demonstrated.

Let's finish by once more contrasting this with the ID position. Given that ID is merely a 'inference' of design which is baseless without any detail concerning the designer, the mechanisms of the design, the timeframe of the design or the intentions of the designer, there is literally nothing we can pull out of here in order to make predictions or perform tests. Even Kiplings fantastical Just So Stories are theoretically testable. ID can't even claim that.

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