Effect Of Lexa On Chromosomal Integration Of Ctx Phi In Vibrio Cholerae

The genesis of toxigenic Vibrio cholerae involves acquisition of CTX phi, a single-stranded DNA (ssDNA) filamentous phage that encodes cholera toxin (CT). The phage exploits host-encoded tyrosine recombinases (XerC and XerD) for chromosomal integration and lysogenic conversion. The replicative genome of CTX phi produces ssDNA by rolling-circle replication, which may be used either for virion production or for integration into host chromosome. Fine-tuning of different ssDNA binding protein (Ssb) levels in the host cell is crucial for cellular functioning and important for CTX phi integration. In this study, we mutated the master regulator gene of SOS induction, lexA, of V. cholerae because of its known role in controlling levels of Ssb proteins in other bacteria. CTX phi integration decreased in cells with a Delta lexA mutation and increased in cells with an SOS-noninducing mutation, lexA (Ind(-)). We also observed that overexpression of host-encoded Ssb (VC0397) decreased integration of CTX phi. We propose that LexA helps CTX phi integration, possibly by fine-tuning levels of host-and phage-encoded Ssbs.