The genesis of toxigenic Vibrio cholerae involves acquisition of CTX, a single-stranded DNA (ssDNA) filamentous phage thatbencodes cholera toxin (CT). The phage exploits host-encoded tyrosine recombinases (XerC and XerD) for chromosomal...
moreThe genesis of toxigenic Vibrio cholerae involves acquisition of CTX, a single-stranded DNA (ssDNA) filamentous phage thatbencodes cholera toxin (CT). The phage exploits host-encoded tyrosine recombinases (XerC and XerD) for chromosomal integration and lysogenic conversion. The replicative genome of CTX 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 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 integration decreased in cells with a 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. We propose that LexA helps CTX integration, possibly by fine-tuning levels of host- and phage-encoded Ssbs.
