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Cells defective for replication restart undergo replication fork reversal
Author(s) -
Grompone Gianfranco,
Ehrlich Dusko,
Michel Bénédicte
Publication year - 2004
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400167
Subject(s) - recbcd , holliday junction , biology , microbiology and biotechnology , dna replication , mutant , replication (statistics) , genetics , replication factor c , dna , control of chromosome duplication , dna repair , gene , virology
We have studied the fate of blocked replication forks with the use of the Escherichia coli priA mutant, in which spontaneously arrested replication forks persist owing to the lack of the major replication restart pathway. Such blocked forks undergo a specific reaction named replication fork reversal, in which newly synthesized strands anneal to form a DNA double‐strand end adjacent to a four‐way junction. Indeed, (i) priA recB mutant chromosomes are linearized by a reaction that requires the presence of the Holliday junction resolvase RuvABC, and (ii) RuvABC‐dependent linearization is prevented by the presence of RecBC. Replication fork reversal in a priA mutant occurs independently of the recombination proteins RecA and RecR. recBC inactivation does not affect priA mutant viability but prevents priA chronic SOS induction. We propose that, in the absence of PriA, RecBC action at reversed forks does not allow replication restart, which leads to the accumulation of SOS‐inducing RecA filaments. Our results suggest that types of replication blockage that cause replication fork reversal occur spontaneously.