Multiple pathways process stalled replication forks

AUTOR(ES)

Michel, Bénédicte

FONTE

National Academy of Sciences

RESUMO

Impairment of replication fork progression is a serious threat to living organisms and a potential source of genome instability. Studies in prokaryotes have provided evidence that inactivated replication forks can restart by the reassembly of the replication machinery. Several strategies for the processing of inactivated replication forks before replisome reassembly have been described. Most of these require the action of recombination proteins, with different proteins being implicated, depending on the cause of fork arrest. The action of recombination proteins at blocked forks is not necessarily accompanied by a strand-exchange reaction and may prevent rather than repair fork breakage. These various restart pathways may reflect different structures at stalled forks. We review here the different strategies of fork processing elicited by different kinds of replication impairments in prokaryotes and the variety of roles played by recombination proteins in these processes.

Documentos Relacionados

• RecA protein promotes the regression of stalled replication forks in vitro
• Stabilization of stalled DNA replication forks by the BRCA2 breast cancer susceptibility protein
• PARP is activated at stalled forks to mediate Mre11-dependent replication restart and recombination
• BLM and the FANC proteins collaborate in a common pathway in response to stalled replication forks
• Sir2p suppresses recombination of replication forks stalled at the replication fork barrier of ribosomal DNA in Saccharomyces cerevisiae