Smarter than the average phage.

The seventh cholera pandemic emerged in the poorer nations of the world towards the end of the 20th century and continues to kill thousands of people per year. The causative agent of cholera, the Gram-negative bacterium Vibrio cholera, is only pathogenic when it contains a lysogenic bacteriophage, CTXphi, that encodes the toxin responsible for inducing massive fluid loss from the human host. Site-specific integration of CTXphi into chromosome I of V. cholera occurs at a site, dif, that is normally required for resolution of chromosome dimers generated by homologous recombination. An article in this issue of Molecular Microbiology reports the analysis of interactions between two host encoded recombinases, XerC and XerD, and the recombination sites involved in lysogeny. Surprisingly, recombination between the CTXphi attP site and the chromosomal dif site requires additional recombinase binding sites, downstream from the positions of strand exchange, which might play an architectural role. The positions of strand cleavage also differ significantly between the two sites, suggesting a novel recombination mechanism that implicates additional host factors in resolution of the Holliday junction intermediate.