Yesterday I gave another talk, this one to the Biodiversity Centre in-house series. It was an evolution-focused version using my standard "Do bacteria have sex?" framework. This morning I realized that there's a point I should be making every time I use this framework.
Rather than describe the whole talk I've posted the slides to Slideshare (you can see them here). But you won't need to look at them to understand the point of this post. Early in these talks I always explain that, in bacteria, transfer of chromosomal genes between close relatives can occur by any of three 'parasexual' processes - conjugation, transduction and transformation. Incorporation of transferred alleles into the chromosome requires homologous recombination, mediated by an assortment of enzymes in the recipient cell. Then I describe the evidence that conjugation and transduction occur as unselected side effects of genes on parasitic genetic elements (plasmids and phages respectively) - the selected functions of these genes are infectious transfer of the parasites. And the evidence that all the enzymes that contribute to recombination have been selected for functions in DNA replication and repair, with no evidence of selection for the recombination effects.
At this point I have always next explained that transformation is thus the only bacterial process that still could have evolved for a sexual function (to promote recombination of chromosomal genes). But today I realized that I should first point out that this means that E. coli doesn't have sex, because E. coli is one of the many bacteria that don't have natural transformation.
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3 weeks ago in Genomics, Medicine, and Pseudoscience
Oh noes, everything we were taught about bacteria in intro genetics comes crashing down in flames! Well, the sex aspect of it anyway...
ReplyDeleteEnjoyed your talk, by the way!
I was wondering whether by analysing the relatives of H.influenzae one could detect a gradual progression of accumulating uptake sequences in the genome as the US specificity intensified due to whatever changes in the uptake machinery? Although I guess it may also be that this favouring of sequences could happen quite rapidly if all it takes is one kink in the uptake channel to develop bias... Also could the two groups of bacteria that exhibit US bias have had some mechanism to initially compensate for the presumably poorer uptake efficiency (and thus, greater vulnerability for starvation); or is uptake efficiency ultimately unaffected by sequence specificity?
I have a 2006 paper that addresses some of these qestions (Redfield et al, BMC Evolutionary Biology). But the frequency of uptake sequences at equilibrium will depend on how often the cells take up homologous DNA (in their natural environment) and how often this recombines with the chromosome, so we can't directly infer the strength of specificity.
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