Survival of the Fittest

Vriezen JAC, Valliere M, Riley MA. 2009. The evolution of reduced microbial killing. Genome. Biol. Evol. 2009:400-8.

One interesting question in the plasmid world is how to classify plasmids. They are commonly compared to parasites in that they require the use of host machinery for replication and protein production, and can “infect” bacterial hosts even if this reduces host fitness (i.e. the bacteria often have no say in whether a plasmid is admitted into its cell or not). Unlike parasites, however, plasmids can be beneficial to their hosts, depending on what genes they code for and the current environment. For instance, some plasmids code for colicin production, which can kill bacteria that are closely related to the host bacteria(1). This gives plasmid-bearing bacteria an edge on competing strains, but at a slight cost due to plasmid maintenance and colicin production. In this article the authors found that after 253 generations of growth in the absence of competing strains, the killing ability of E. coli was reduced in an attempt to reduce the cost of plasmid maintenance in an environment wherein colicin production is unnecessary.

So far, these results aren’t terribly surprising: if colicin production comes with a cost the bacterial host then any bacterium that can reduce this cost will be at a selective advantage. This will allow bacteria with reduced killing affects to become more dominate in the population over time(c.f. 2,3). What is more interesting is that, even though it is the plasmid that codes for colicin production it is the bacteria’s genes that change to reduce colicin production. After 253 generations the plasmid’s sequence remained completely unaltered, whereas the expression of host genes including those for DNA repair, Mg ion uptake, and late prophage genes displayed changes in their regulation. The authors commented that this was also a wider variety of genes that were involved in this evolutionary response to colicin production pressures than expected.

The interactions between plasmids and their host bacteria appear very complex. The fate of each is closely related to the fate of the other, and there are a variety of ways that the plasmid, the host, or both could change to increase the chances of survival of both together. Changes on one partner, in this case the bacteria, can regulate the expression of the other without altering the other at all. The interactions and coevolution of plasmids and bacteria are dynamic, with countless possibilities that have yet to be explored. What seems ever more clear with each such study is that when faced with a problem, in the words quoted in Jurassic Park, “Nature will find a way.”

Julie Hughes
University of Idaho

References\Further Reading:

1. Cascales E, et al. 2007. Colicin biology. Microbiol Mol Biol Rev. 71:158–229.

2. Lenski RE, Winkworth CL, Riley MA. 2003. Rates of DNA sequence evolution in experimental populations of Escherichia coli during 20,000 generations. J Mol Evol. 56:498–508.

3. Modi RI, Adams J. 1991. Coevolution of bacterial-plasmid populations. Evolution. 45:656–667.

4. Walker D, et al. 2004. Transcriptional profiling of colicin-induced cell death of Escherichia coli MG1655 identifies potential mechanisms by which bacteriocins promote bacterial diversity. J Bacteriol. 186:866–869.