I'll be giving a talk at the upcoming meeting of the Society for Molecular Biology ad Evolution (SMBE) in Halifax. The focus of the session is on the evolutionary consequences of the mechanisms that cause recombination, and I'll be talking about how the sequence specificity of the H. influenzae DNA uptake machinery has affected the evolution of its genome and proteome.
I'm going to start the talk by describing what usually happened at the end of the talks I used to give on the regulation and evolutionary function of competence. I'd conclude that the regulatory evidence supported the hypothesis that bacteria take up DNA for food, not for its genetic information. Most people find this a very unwelcome idea, and one of the first questions would always be why I thought the uptake specificity wasn't compelling evidence that bacteria take up DNA to get new genetic information. I'd answer by saying that uptake specificity needn't have evolved to promote recombination, and that we were beginning to investigate alternative explanations.
I'm hoping that this introduction will capture people's attention - "There's a controversy! Everyone thinks she's wrong!"
We now have tons of analyses to report: the Perl model of USS evolution, the uptake assays with mutated USSs, the Gibbs motif analyses, the reading frame analysis, the evidence that USSs are not insertion elements but motifs that arise by mutation, the correlation of uptake specificity with Pasteurellacean phylogeny, the lack of coding constraints due to the USS int he H. influenzae genome, the presence of competence genes and genomic USSs across the Pasteurellaceae (including species that can't be transformed in the lab)... Unfortunately for me (fortunately for my audience?) I only have 30 minutes including the question period. I'm going to try to pull a draft talk into shape for Monday, when it will be my turn to do lab meeting.
A Magnolia experiment
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