Survival of the fittest: a role for phage-encoded eukaryotic-like kinases.

Phages are often thought of as mortal enemies of bacteria. This dynamic relationship has led to the evolution of a number of processes in bacteria designed to defeat these attacks. Examples of these include blocking phage attachment, CRISPR, and restriction modification systems. Temperate phages provide another source of protection by excluding infection of heterologous phage, thwarting phage production and further infection. This strategy protects the rest of the bacterial population from attack. The lambdoid phage 933W, a source of the genes encoding Shiga toxin in the highly pathogenic O157:H7 enterohemorrhagic E. coli strain, also carries a gene encoding a eukaryotic-like tyrosine kinase, Stk. In this issue of Molecular Microbiology, Friedman et al. (2011) show that Stk, through its kinase activity, excludes infection by another lambdoid phage HK97. This exclusion is very specific as it does not affect a number of other lambdoid phages. HK97 contributes to its own demise by expressing the product of an open reading frame, orf41, which is required for Stk activation. The authors further show that autophosphorylation increases the stability of Stk and suggest that autophosphorylation contributes to Stk activity. Whether or not this exclusion activity provides a selective advantage through maintenance of Stk activity is yet to be explored.