Scientist doping

I am currently sitting in on an ethics class because NIH requires that I do so if I want to accept their funding. I had an ethics class as a graduate student and we talked about all of the usual things like stem cell research, gene therapy, experimentation with animals, etc. The ethics class I am in now is a bit different, which is nice because I can think about some new issues. The issue up for discussion yesterday was sports doping, which is when athletes take drugs to enhance their natural abilities. Most people find this unethical because athletes should perform using only what is available to them naturally. Enhancement is considered to be unfair and a sign of bad sportsmanship. But I couldn't help but compare the enhancement of athleticism using steroids to the enhancement of brain power/alertness using caffeine. Every day I enhance my alertness by drinking tea or coffee. Does this mean that I have an unfair advantage in science because I am doping my brain with caffeine? I would say no but only because the majority of scientists I know rely on caffeine themselves. Basically, we are all enhancing our natural abilities. But no one has a problem with this. So I guess caffeine enhancement of scientists is not as unethical as steroid enhancement of athletes. Why is this?

Recombination

In my previous post I eluded to the lack of resolution in the H. influenzae phylogeny. I have now attempted to use three different methods of phylogenetic reconstruction (maximum likelihood, distance, and parsimony) and, due to some characteristics of the datasets, only parsimony was feasible. From the whole genome alignments I had 101 alignment files. A phylogeny was inferred for each of these alignment files using parsimony and 100 bootstrap pseudoreplicates. Most clades in each of these topologies had poor bootstrap support. Then, a consensus tree was inferred from each of the 101 trees. Guess what? Absolutely no resolution of any clades, nothing, a "star" phylogeny.

Is it due to recombination? Probably. I tested for recombination using a parsimony based approach (Bruen et al. 2006. Genetics 172:2665) in each of the 101 alignment files (so within each alignment region, not between alignment files) and found that only 11 alignment files did NOT have evidence of recombination. The lack of recombination in all but one of these is probably due to the small size, most of the 11 were under 1 kb.

What does this all mean? Recombination was previously thought to be rare in H. influenzae, based on linkage between phenotypes and multi-locus enzyme electrophoresis types. But sequence data is changing what we know about the population structure of H. influenzae. MLST studies have already shown modest incongruence between gene trees and fancy Bayesian statistics have shown that the recombination rate is moderate. My work is now showing that recombination occurs often enough to obliterate phylogenetic signal. My next question is: is it mostly due to transformational recombination?