XerD-mediated FtsK-independent integration of TLC? into the Vibrio cholerae genome.

ABSTRACT: As in most bacteria, topological problems arising from the circularity of the two Vibrio cholerae chromosomes, chrI and chrII, are resolved by the addition of a crossover at a specific site of each chromosome, dif, by two tyrosine recombinases, XerC and XerD. The reaction is under the control of a cell division protein, FtsK, which activates the formation of a Holliday Junction (HJ) intermediate by XerD catalysis that is resolved into product by XerC catalysis. Many plasmids and phages exploit Xer recombination for dimer resolution and for integration, respectively. In all cases so far described, they rely on an alternative recombination pathway in which XerC catalyzes the formation of a HJ independently of FtsK. This is notably the case for CTX?, the cholera toxin phage. Here, we show that in contrast, integration of TLC?, a toxin-linked cryptic satellite phage that is almost always found integrated at the chrI dif site before CTX?, depends on the formation of a HJ by XerD catalysis, which is then resolved by XerC catalysis. The reaction nevertheless escapes the normal cellular control exerted by FtsK on XerD. In addition, we show that the same reaction promotes the excision of TLC?, along with any CTX? copy present between dif and its left attachment site, providing a plausible mechanism for how chrI CTX? copies can be eliminated, as occurred in the second wave of the current cholera pandemic.

SUBMITTER: Midonet C 

PROVIDER: S-EPMC4250166 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature