Friday, 25 October 2013



Viruses are the main killers of bacteria. However, bacteria increasingly get resistant to multiple strains of viruses. Thus, there is a trade-off between viral-induced bacterial mortality and bacterial resistance against viruses. Apart from mortality, viruses also induce evolution and diversification of bacteria via multiple processes. Both the bacteria and their viruses influence evolution of each other. In other words, they co-evolve continuously where the host bacteria evolve resistance against viruses and viruses evolve in order to conquer host’s resistance. Thus, it is a microbial arms race or an antagonistic co-evolution.  
This study investigated co-evolution between Synechococcus (key primary produces of the marine environment) and cyanophages (myoviruses). Significant co-evolutionary cycles between Synechococcus and cyanophages, were observed by the authors. This includes Synechococcus evolving resistance against the cyanophage which subsequently conquer the resistance of evolved Synechococcus and so on..., in such a way persistence of an antagonistic co-evolutionary cycle.
Authors noted that although, genotypes of both the hosts and its viruses were altering together (co-evolving), the phenotypic diversity of the host Synechococcus was greater than the viruses. Authors also found that co-occurring host phenotypes had different viral-resistance capabilities. They linked this to the fitness cost of viral resistance, previously reported in both the   Synechococcus and Prochlorococcus.
Surprisingly, genome sequencing of the evolving viruses could not find mutations in the tail fiber genes, implicated in determining the host range. Rather, half of the mutations occurred in another gene of unknown functions which could be involved in the host-viral interactions. As significant mutations were detected in that gene, in numerous tested viruses; authors suggested that it could be under strong positive selection pressure. It might be involved in determining the viral host range. Nevertheless, they argued that multiple genes in addition to this one might be involved in the host range determination.   
Adaptive mutations were observed in the Synechococcus genome. Viral resistance is an intricate trait, involving multiple loci of the Synechococcus. Remarkably, they evolved resistance to some viruses in multiple ways. In other words, mutations in totally different genes provided resistance to the same virus. This finding which was not observed in viruses, support the hypothesis that parallel evolution within a gene arises more frequently in bacteriophages, compared to their hosts.
To test the relevance of this experimental study to the viral-host co-evolutionary patterns occurring in nature, authors challenged the evolved population of Synechococcus with the genetically distinct myoviruses isolated from Rhode Island waters and found Synechococcus cells getting resistant to them, over a period of time. Pleiotrophy was observed in the Synechococcus population.  Resistance to one virus also provided resistance to other viruses whereas some of them showed opposite trend where getting resistant to one virus concurrently made them susceptible to other viruses.
Overall, this study explores antagonistic co-evolution between bacteria (Synechococcus) and their bacteriophages, highlighting its complexity. Particularly, it underlines how bacteria and their viruses change continuously in order to conquer each other and in doing so generate and sustain diversity of these key primary producers and also their viruses. Additionally, this co-evolution has potential implications in understanding viral activity in the oceans’ nutrient cycling.  

Marston M.F., Pierciey F.J., Shepard A., Gearin G., Qi J., Yandava C., Schuster S.C., Henn M.R. & Martiny J.B.H. (2012) Rapid diversification of coevolving marine Synechococcus and a virus; Proceedings of the National Academy of Sciences, 109(12):4544-4549.


  1. Do you think that this paper has a possible link to the point made by Denis Noble (evolution module), that one gene doesn't necessarily code for one phenotype, shown by the change in several genes influencing the resistance to just one virus?

    1. Hi Ethan, thanks for your comment.

      As this paper also pointed out, viral resistance is a very complex process, involving multiple genes. Thus, it is difficult to directly say that this paper has a direct link to Denis Noble;s ideas about evolution.
      Recently, I was reading a book "recombinant DNA genes & genomes" by Watson et al. 2007. It is really good for understanding basics of genetics & epigenetics.
      Bacteria usually have operons - groups of genes that are regulated together, as a group. This could be related to genes of viral resistance.
      Again, viral resistance may not necessarily contain role of mutations (change in DNA sequence) of bacteria at all. DNA methylation and activity of restriction enzymes like restriction endonuclease on non-methylated phage DNA is I guess an immune pathway that bacteria uses against phages.
      RNA interference - newly found way of regulating gene expression is believed to have evolved for silencing viruses. But I cannot say if this plays any role in bacteria getting resistant against their phages.

      As far as, Denis Noble's thinking that one gene doesn't necessarily code for one phenotype - that is undoubtedly true, I think.
      Genes (at least eukaryotic genes) are made up of introns (non-coding sequence) and exons (coding sequence). In making proteins, only exons are used. But at transcription, mRNA consists of both introns and exons. RNA splicing is a process between transcription and translation that removes non coding introns. Watson et al. 2007 have provided good evidence for alternative splicing in which introns involve in shuffling exons, thus shuffling the mRNA sequence and which codes totally new protein from the same DNA sequence or gene. This is why, in human genome project, genes identified are around 22000 whereas gene transcripts found are 35845. Alternative splicing and presence of introns make it very clear that "one gene equals one protein is hardly true" There are few examples (given by Watson et al. 2007) for genes encoded within other genes (Watson et al. 2007). This is very complicated area, very different from the topic of the above paper.