| Recombinational DNA repair is the major function of homologous recombination in bacteria. Replication forks become frequently inactivated at various barriers, even in the absence of exogenous DNA damage. Therefore, resuscitation of inactivated replication forks through homologous recombination is an important housekeeping function in all cells.; Replication fork regression is a major pathway to rescue stalled forks, allowing nonmutagenic bypass of DNA lesions. We show here that both Escherichia coli RecA and RecG proteins can promote regression of a branched DNA substrate that mimics a possible structure of a stalled replication fork. The mechanisms of action of the two proteins are different, but both require ATP hydrolysis. When RecA and RecG proteins are incubated together with the DNA substrate, they did not counteract each other under optimal conditions for both. Only high RecG levels inhibit the RecA-promoted fork regression. These results may provide some insight into the role of these proteins in rescuing stalled replication forks in vivo. |
