Applications of Common Descent

I've seen a lot of good arguments for evolution (and some pretty shoddy ones). Most hinge on one of two things: either the evidence for evolution, or the scientific nature of the model (as compared to the alternatives). At one point, I got curious as to whether there was a different approach. I posted about this to the convert_me lj community. While much of the subsequent discussion was off topic, I did get some interesting leads, and did the appropriate research to come up with a with a followup post, which, in turn, is the basis for this page.

There are various applications I discarded. Almost everything to do with single-celled organisms was unacceptable because proponents of ID generally agree that microevolution happens (the distinction between micro and macro evolution is not something most scientists agree with, but this is not meant to be targeted at scientists). Second, areas for which evolution was a motivator, but not necessary (such as understanding the genetic code), did not fit my criteria, because that research could have been motivated by ID theory.

In essence, I was looking for research which depends on the model of common descent (beyond that within a species) and for which there have been real world applications. I was also particularly interested in applications which were not already commonly discussed.

So, here are real world applications of the theory of common descent.

Given the EV model above, a genetic defect can be introduced at some point and propagate to its children. Then, if we notice a defect among several modern animals (e.g. G and H), it is possible to do a search across species to localize when this problem was introduced (if it occurs in G, H and D, it could have originated at B), identify where in the genetic code it is (by comparative genetic analysis), and how to circumvent it.

This was used in the investigation of an absence of an enzyme that produces ascorbic acid. This lack is the underlying cause of scurvy. The (previously thought to be human-only) disease was found in a guinea pig around 1907, which caused a search which found the defect to also occur in some monkeys, but not other mammals. Further searches narrowed down the boundary, which led to an estimate of where and when the defect originated in evolutionary history. This helped explain why the disease exists. Examining the lifestyle of the species affected by it changed the accepted ideal doses of vitamin C. Further: knowing which species are similar but do not have the defect can allow it to be removed from human genetic code in the future. (Just think - our progeny may no longer need to eat those healthy fruits and vegetables.) This area of research is nonsensical if you do not believe in common descent. A design would either have the defect or not - so either all the animals would be affected or they would not be. A subsequent mutation could cause some of the animals to have the defect, but it would not be grouped within evolutionary history by a common ancestor. Therefore, the line of inquiry would not have been pursued, and the medically helpful information would not have been discovered.

Currently, one of the most difficult problems in biology is mapping genetic function, typically by finding out how a gene maps to a protein. Understanding this is key to figuring out solutions to genetic problems. This has been extremely challenging because of the complexity of the models involved, and there has been no way to simulate protein structure based solely on the genetic string.

Recently, however, there has been some success in identifying key genetic elements by comparative genetic analysis. The genetic strings that represent similarly functioning proteins within various animals are compared. Based on the evolutionary distance between the animals, it is possible to analyze which parts of the genes change quickly, and which change more slowly. (If you compare G, H, and D above, then there is more 'distance' between G and D than between G and H, and knowing the common ancestor allows the estimation of rate of change.) The genes that change more slowly are the ones that are more key to the way the corresponding protein folds and functions. Using this method, it has been possible to isolate gene sequences commonly responsible for folding, which resulted in some success in predicting via simulation what a protein looks like based on the gene sequence. (Jonathan A. Eisen and Martin Wu, 2002. "Phylogenetic Analysis and Gene Functional Predictions: Phylogenomics in Action", Theoretical Population Biology 61)

Again, this is an area of research that is nonsensical with the ID model. There, the genetic distance between species is absolute - based on the original design plus mutation since then, so there is no way to get a sequence of gradually diverging gene sequences and no reason to pursue this line of inquiry.

If the common descent model is accepted, organs whose function is unknown can be assessed through comparative anatomy, and we can decide whether or not it is harmful to mess with certain parts of our bodies. In humans, the appendix, wisdom teeth and coccyx are fairly commonly removed when they cause problems. It is understood that it is safe to do so because we understand the origins of the organs, and thus their lack of functionality. If the common descent model is not accepted, we do not have that rationale for removing these organs, so would not so lightly be able to proceed with such surgeries. In that way, the evolution model is medically useful. (The converse is true: we can understand functional organs through comparative anatomy, but this meshes with template reuse in ID theory, so is not a good argument.)

These are some examples I discarded as not being sufficiently strong. If there is a way to strengthen any of them, that would be great, but for now, I think they will be easily taken apart by a someone prepped for them or someone of reasonable intelligence.
Feedback
If you want to respond to any of these (either way), you can email me, contact me via the contact page or respond to the livejournal post. I am particularly interested in the following questions:

Are these arguments (or would they be) particularly when talking to a layman? If not, could they be made? Could they in general be improved, and how do they compare to the typical arguments from the nature of science? Given the examples, can you think of other ways the model has been used?

For those who favor various flavors of ID theory, do you have counter arguments to these points? Are there weaknesses here that were not listed?

Thanks to those who made suggestions in the lj threads particularly lowk for a sequence of references, tom_kbel for various suggestions below, and scorpy1 for the ascorbic acid article.