Loss of both Holliday junction processing pathways is synthetically lethal in the presence of gonococcal pilin antigenic variation.

ABSTRACT: The obligate human pathogen Neisseria gonorrhoeae (Gc) has co-opted conserved recombination pathways to achieve immune evasion by way of antigenic variation (Av). We show that both the RuvABC and RecG Holliday junction (HJ) processing pathways are required for recombinational repair, each can act during genetic transfer, and both are required for pilin Av. Analysis of double mutants shows that either the RecG or RuvAB HJ processing pathway must be functional for normal growth of Gc when RecA is expressed. HJ processing-deficient survivors of RecA expression are enriched for non-piliated bacteria that carry large deletions of the pilE gene. Mutations that prevent pilin variation such as recO, recQ, and a cis-acting pilE transposon insertion all rescue the RecA-dependent growth inhibition of

SUBMITTER: Sechman EV 

PROVIDER: S-EPMC2612780 | biostudies-literature | 2006 Jul

REPOSITORIES: biostudies-literature