My turn to do lab meeting

I've been so absorbed in my Useful Genetics course that I've let our weekly lab meetings lapse over the last few months.  But I've set up a new schedule and today it's my turn to present.  Of course I haven't done any experiments lately, but I've done one tiny analysis and I'll also talk about plans for the CIHR proposal.

The tiny analysis was the first step in addressing a question I've been wondering about for a while now- the phylogenetic distribution of the rec2/comEC gene.  In H. influenzae the  Rec2 protein sits in the inner membrane and translocates a single strand of DNA from the periplasm to the cytoplasm.  Its Bacillus subtilis homolog ComEC does the same thing at the one cytoplasmic membrane. 

Homologs of these proteins are present in all known competent species, and the appropt=riate experiments have been done they have the same DNA-translocation function, are competence-regulated, and do not have any other obvious function in the cell.  This distinguishes them from all the other proteins consistently required for DNA uptake, which are members of the type 4 pilus complex and known to also function in other pilus-associated processes.

Thus the phylogenetic distribution of rec2/comEC might be expected to reflect the phylogenetic distribution of competence.  But as far as I know nobody has examined this.

Before I describe what I found, I should bring up the distribution of another competence-induced gene, dprA.  I've written about dprA here and here; it doesn't contribute to DNA uptake but protects incoming DNA from nuclease degradation and promotes homologous recombination with the chromosome.  I previously discussed the phylogenetic distribution of dprA; it's very widespread and highly conserved across a wide range of bacteria not known to be competent, so I argued that it must have another function that's independent of promoting homologous recombination of incoming DNA in competent cells.  I was leaning to the idea that 'competence-regulons' include not only DNA uptake machinery but machinery to mitigate other harmful consequences of nucleotide scarcity, especially stalling of replication forks.

Back to rec2.  My tiny analysis was to take a first look at the distribution of rec2.  All I did was ask Gen Bank to search for rec2 and for comEC.  As controls I used dprA and recA.  GenBank helpfully provides a tree-view summary of what it finds, and that's all I've looked at.  Here are the results of the four searches:

 

First conclusion:  rec2/comEC homologs are present in many many bacterial genomes than there is any evidence of competence for, including some that have been shown to not take up DNA.  This could have one of two interpretations.  First, it could mean that many many more bacteria are naturally competent, and that competence is likely ancestral to all bacteria.  Or, it could mean that rec2/comEC has another function in the cell, one that's independent of the ability to take up DNA.  

Note the similarlty of the comEC and dprA distributions.  (I suspect that most of the rec2 hits are also included in the comEC results.)  I had only been thinking of the first interpretation for rec2/comEC, but had previously taken the second interpretation for dprA. But now I think I need to consider both interpretations for both genes.