About that Meyer, 2012 study


(Cornelius_Hunter) #1

We have talked about the Meyer, 2012 paper from Lenski’s group where the phage adapted to use OmpF as a receptor. Quite a few trials were run, and the sequence of mutations in the virus protein J were tracked. Interestingly, zero synonymous mutations were found. As the paper explains:

First, all 248 independent mutations in the 51 sequenced J alleles were nonsynonymous, whereas the expected ratio of nonsynonymous to synonymous changes is 3.19:1 under the null model for the ancestral J sequence. This great excess is evident even if we include only the 82 nonsynonymous mutations in the 24 isolates that did not evolve the new receptor function.

I wonder if anyone can explain why there there were zero synonymous mutations?

The paper presents this fact as evidence for strong selection, which I think is clearly a strained argument. So what’s going on?


(Benjamin Kirk) #2

No drift, because drift predicts synonymous mutations.


(Cornelius_Hunter) #3

Well I think it actually makes sense. There would be many synonymous mutations in the populations, but since the experiment sampled only a tiny fraction of the viruses, they would mainly only see mutations that are fixed, and on such a short timeline, those would only be selected mutations.