Monday 31 December 2012


Rapid diversification of coevolving marine bacteria Synechococcus and a virus

Viral lyses of bacteria play a key role in the cycling of nutrients in the ocean. This said, our understanding of how phenotypic plasticity between bacteria and viruses influences the biogeochemical cycling of nutrients is limited. Marston et al (2012) investigated how the phenotype and genotype of Synechococcus sp. WH7803 and the Myoviridae virus RIM8 may change when incubated in a chemostat experiment for six months. Marston e al (2012) aimed to answer three questions during this investigation. Firstly, what is the potential for coevolution and diversification in Synechococcus and RIM8? Secondly, are there candidate genes that underlie the phenotypic diversification? Thirdly, do mutations that arise from pair wise coevolution exposures have consequences for interactions with other Synechococcus and and cyanophage strains?

Marston t al (2012) preformed four replicate chemostat experiments and one control. To test for the potential of antagonistic coevolution to lead to the diversification of Synechococcus and RIM8 single cells and viruses were isolated from each of the chemostats by colony isolation and plaque purification at six time points over the six month investigation. Infection assays were conducted to determine the ability of the viral isolates to infect various Synechococcus isolates from the same chemostat.

Over the six months up to 13 viral and 4-11 bacterial phenotypes were isolated from the chemostats indicating that antagonistic coevolution is possible between these two strains. In both cases the phenotypic change was directional. The viral infectivity increased over time, such that viruses from the later time points had a wider host range than earlier time points.  Similarly, Synechococcus increased its resistance to viral infection over the course of the experiment. The development of phenotypes over time differed between RIM8 and Synechococcus. Viral phenotypes appeared to replace one-another over time, whereas, Synechococcus showed multiple phenotypes at any one time point. Marston et al (2012) suggests that the actual number of Synechococcus phenotypes present in the investigation may have been greatly under estimated because the low number of isolates taken at each time point.  The identification of the genes controlling the changes phenotype is complex in this investigation. Although obvious changes were observed in amino acid sequence it did not always lead to the same phenotype. In one example, on day 84 the RIM8 virus was shown to have the same amino acid sequence but this represented five different phenotypes. Synechococcus also showed similar complexity. It appeared that different genes controlled the resistance response to the same virus.

In the third part of the experiment the authors wanted to see how the evolved Synechococcus would react to 31 different strains of viruses isolated from seawater in an attempt to make the results more realistic. The results showed that the resistance increased with time, but also, that the increased resistance to viruses was pleiotropic- resistance to one virus lead to resistance to other similar viruses. The opposite is also possible, with resistance to one increasing the susceptibility to other viruses. In this study increasing resistance to RIM8 lead to increased sensitivity to RIM26.

I chose this investigation because I believe it highlights some of the complexities in how marine bacterial/virus interaction evolves and how dynamic it is. I also thought it was interesting how the same amino acid sequence can produce differing phenotypes in such simple organisms, leading to differing levels of resistance, either positive or negative.   

 

 Marston.M. F., Peirciery. F. J., Sherperd. A., (2012). Rapid diversification of coevolving marine Synechococcus and a virus. PNAS. 109. 12. 4544-4549.
http://www.pnas.org/content/109/12/4544.full

1 comment:

  1. Matt - a very interesting experimental study made possible by the ability to perform full genome analysis of viral and host at various stages. Are there any clues about which host and virus genes are most likely to show mutations that are selected?

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