The Colicin Plasmid Persistence Problem

Yesterday, I described an interesting paper that provides a potential solution to the plasmid persistence problem–how do bacterial mini-chromosomes that can jump from bacterium to bacterium survive? Not only does this paper shed some light on the ‘plasmid persistence problem’, but it also has some nice data regarding the evolution of colicin plasmids, which are near and dear to the Mad Biologist’s heart. Colicin plasmids carry a gene that produces an antibacterial toxin, the colicin, (essentially, an antibiotic) as well as a gene that confers immunity to that same colicin and only that specific colicin (there are around 20 different types of colicins). Colicin plasmids definitely impose a cost on the bacterium: for the toxin to be released, the cell has to explode (there’s a plasmid-encoded gene for that too).

Colicin plasmids are perplexing because of the phenomenon of resistance: this is a chromosomal mutation that confers resistance to multiple colicins. In fact, most E. coli are resistant to most colicins, yet anywhere from 5-33% of E. coli (depending on where you look) have colicin plasmids.

In the paper, the authors found that the p2 plasmid in Salmonella (which is what they used in their experiments) encoded all of the colicin-related genes. When they removed the colicin genes from the plasmid, they found that the plasmid wasn’t as common in the remaining E. coli as when the plasmid had the colicin genes. They conclude:

Furthermore, we found that the plasmid-encoded cib/imm [colicin] genes do enhance the recipient’s fitness, in particular if the recipient strain has originally been sensitive to the colicin. In mammalian host populations, diarrheal infections do occur multiple times per year suggesting that enterobacterial-blooms do occur at appreciable frequency. In these situations, cib/imm genes do confer a significant (but locally confined) fitness benefit (protection from colicin-killing; advantage against colicin-sensitive competitors) and may foster plasmid maintenance in selective sweeps. Thus, conjugative transfer during episodes of disease inflicted bacterial blooms may explain why so many conjugative plasmids from enterobacterial species do encode colicins and the respective immunity proteins.

As I mentioned yesterday, we have to approach this from a non-equilibrium perspective. Colicin plasmids will occasionally find themselves in the presence of a colicin sensitive strain even though most strains are colicin resistant. If, for whatever reason, such as the Salmonella infection reported in the paper, that strain can sweep to high frequency, the added benefits of the colicin-related genes will make maintenance of the plasmid more likely. While this would seem to be a relatively rare event, in non-human affected systems, colicin plasmids appear to be stable and don’t jump around all the time, which is what we would expect under a regime of lots of very localized sweeps–most of the end results of those sweeps will become extinct because they are very localized.

I haven’t come across a paper that’s made my think about plasmid evolution like this in a long time. Now if this had only been in the main body of the paper and not the supporting information….

Cited article: Stecher B, Denzler R, Maier L, Bernet F, Sanders MJ, Pickard DJ, Barthel M, Westendorf AM, Krogfelt KA, Walker AW, Ackermann M, Dobrindt U, Thomson NR, Hardt WD. 2012 Jan. 9. doi: 10.1073/pnas.1113246109

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