RecF protein targeting to post-replication (daughter strand) gaps II: RecF interaction with replisomes

Author:

Henry Camille1ORCID,Kaur Gurleen23,Cherry Megan E23ORCID,Henrikus Sarah S23,Bonde Nina J1ORCID,Sharma Nischal23ORCID,Beyer Hope A1,Wood Elizabeth A1,Chitteni-Pattu Sindhu1,van Oijen Antoine M23,Robinson Andrew23ORCID,Cox Michael M1ORCID

Affiliation:

1. Department of Biochemistry, University of Wisconsin-Madison , Madison , WI 53706-1544 , USA

2. Molecular Horizons Institute and School of Chemistry and Molecular Bioscience, University of Wollongong , Wollongong, Australia

3. Illawarra Health and Medical Research Institute , Wollongong , Australia

Abstract

Abstract The bacterial RecF, RecO, and RecR proteins are an epistasis group involved in loading RecA protein into post-replication gaps. However, the targeting mechanism that brings these proteins to appropriate gaps is unclear. Here, we propose that targeting may involve a direct interaction between RecF and DnaN. In vivo, RecF is commonly found at the replication fork. Over-expression of RecF, but not RecO or a RecF ATPase mutant, is extremely toxic to cells. We provide evidence that the molecular basis of the toxicity lies in replisome destabilization. RecF over-expression leads to loss of genomic replisomes, increased recombination associated with post-replication gaps, increased plasmid loss, and SOS induction. Using three different methods, we document direct interactions of RecF with the DnaN β-clamp and DnaG primase that may underlie the replisome effects. In a single-molecule rolling-circle replication system in vitro, physiological levels of RecF protein trigger post-replication gap formation. We suggest that the RecF interactions, particularly with DnaN, reflect a functional link between post-replication gap creation and gap processing by RecA. RecF’s varied interactions may begin to explain how the RecFOR system is targeted to rare lesion-containing post-replication gaps, avoiding the potentially deleterious RecA loading onto thousands of other gaps created during replication.

Funder

National Institute of General Medical Sciences

Publisher

Oxford University Press (OUP)

Subject

Genetics

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