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Anticipating chromosomal replication fork arrest: SSB targets repair DNA helicases to active forks
Author(s) -
Lecointe François,
Sérèna Céline,
Velten Marion,
Costes Audrey,
McGovern Stephen,
Meile JeanChristophe,
Errington Jeffrey,
Ehrlich S Dusko,
Noirot Philippe,
Polard Patrice
Publication year - 2007
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601848
Subject(s) - biology , control of chromosome duplication , replisome , helicase , dna replication , ter protein , microbiology and biotechnology , replication factor c , eukaryotic dna replication , genetics , pre replication complex , origin recognition complex , dna repair , minichromosome maintenance , replication protein a , dna , dna binding protein , gene , transcription factor , rna
In bacteria, several salvage responses to DNA replication arrest culminate in reassembly of the replisome on inactivated forks to resume replication. The PriA DNA helicase is a prominent trigger of this replication restart process, preceded in many cases by a repair and/or remodeling of the arrested fork, which can be performed by many specific proteins. The mechanisms that target these rescue effectors to damaged forks in the cell are unknown. We report that the single‐stranded DNA binding (SSB) protein is the key factor that links PriA to active chromosomal replication forks in vivo . This targeting mechanism determines the efficiency by which PriA reaches its specific DNA‐binding site in vitro and directs replication restart in vivo . The RecG and RecQ DNA helicases, which are involved in intricate replication reactivation pathways, also associate with the chromosomal replication forks by similarly interacting with SSB. These results identify SSB as a platform for linking a ‘repair toolbox’ with active replication forks, providing a first line of rescue responses to accidental arrest.