This morning I read and took notes on the Kumar et al. paper. Just to show that I put some effort in, here are my notes:
I learned two sweet things from reading the paper (and doing some google-searching):
1) The proteins responsible for H.influenzae's virulence (i.e. ability to make its host sick) are controlled by a string of repeating DNA nucleotides, such as ATTGCATTGCATTGC... A change in the length of this string can change activate or deactivate certain genes, resulting in new phenotypes and new populations of cells that could survive an antibiotic attack. This is called "phase variation".
2) (The following information is from this site.) Mismatch repair (MMR) is so intense! MMR is a mechanism bacteria (like E.coli) use to fix incorrect base pairing after DNA replication. Basically, MutS binds to a mismatch, it calls over buddy MutL, which gives MutH a kick to get started, which binds to a GATC sequence near the mismatch and cuts the DNA strand there. From this cut to the mismatch, an exonuclease breaks down the DNA, and then DNA polymerase III and DNA ligase fill in the gap.
What is strange is that my ExoI- mutants' transformation frequencies were mucho lower than the published figures. Kumar et al said relative to a value of 1.0 for the transformation frequency of the wildtype, ExoI- got 0.9. I tried this with my figures, and got 0.2 for ExoI-! :\ (My RecJ- number was pretty close, though.)
I'm going to go regrow my streaked double mutants.