Repair and antirepair DNA helicases in Helicobacter pylori.

Abstract:

:Orthologs of RecG and RuvABC are highly conserved among prokaryotes; in Escherichia coli, they participate in independent pathways that branch migrate Holliday junctions during recombinational DNA repair. RecG also has been shown to directly convert stalled replication forks into Holliday junctions. The bacterium Helicobacter pylori, with remarkably high levels of recombination, possesses RecG and RuvABC homologs, but in contrast to E. coli, H. pylori RecG limits recombinational repair. We now show that the RuvABC pathway plays the prominent, if not exclusive, repair role. By introducing an E. coli resolvase (RusA) into H. pylori, the repair and recombination phenotypes of the ruvB mutant but not the recG mutant were improved. Our results indicate that RecG and RuvB compete for Holliday junction structures in recombinational repair, but since a classic RecG resolvase is absent from H. pylori, deployment of the RecG pathway is lethal. We propose that evolutionary loss of the H. pylori RecG resolvase provides an "antirepair" pathway allowing for selection of varied strains. Such competition between repair and antirepair provides a novel mechanism to maximize fitness at a bacterial population level.

journal_name

J Bacteriol

journal_title

Journal of bacteriology

authors

Kang J,Blaser MJ

doi

10.1128/JB.01848-07

subject

Has Abstract

pub_date

2008-06-01 00:00:00

pages

4218-24

issue

12

eissn

0021-9193

issn

1098-5530

pii

JB.01848-07

journal_volume

190

pub_type

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