Vibrio cholerae is abundant in marine and estuarine environments. There are >200 O-antigen serogroups of V. cholerae with only two, O1 and O139, known to cause epidemic and pandemic outbreaks of the disease cholera. Since the 1800s there have been seven cholera pandemics. Each pre-existing pandemic strain is replaced by new diverse strains indicating rapid evolution in this species. Lateral gene transfer (LGT), a two-step process that allows DNA transfer between bacterial cells, has largely driven this rapid evolution. In strains of V. cholerae, at least 20% of genomic content has arisen via LGT with the two most important virulence factors (intestinal adhesin and cholera toxin) present on different mobile DNA elements. In between outbreaks, pandemic strains reside in the marine environment with non-O1/O139 strains. Non-O1/O139 strains act as a significant source of new mobile DNA driving the continued evolution of pandemic strains.
Repair of DNA damage and errors is vital to cell survival. Many biochemical pathways are ubiquitous in cells for the maintenance of DNA integrity. Known repair pathways include, but are not exclusive to: very-short patch (VSP), mismatch repair as well as the inducible SOS response. We have identified a novel 32 kb mobile element in an environmental V. cholerae strain isolated in Sydney, designated S24. The element contains 21 ORFs, many of which are hypotheticals. However, several genes show matches to functions associated with various DNA repair pathways including the three named above. The element encodes a unique recA gene with about 80% DNA identity to other V. cholerae recA genes. Intriguingly, the element has inserted into the resident recA gene, inactivating it. To explore the biological role of this element, we have cloned it into E. coli. The element provides this host with enhanced survival when exposed to UV radiation confirming its role in DNA repair.