Abstract:
:Restart of arrested replication forks is an important process and PriA, the main Escherichia coli replication restart protein, is essential for viability under any condition that increases the frequency of fork arrest. In priA mutant, replication forks are arrested by spontaneously occurring roadblocks and blocked replication forks persist as a result of the defect in replication restart. In the present work, we analysed how recombination proteins contribute to the viability of the priA mutant. RecFOR-mediated homologous recombination occurs in a large fraction of priA mutant cells, indicating a frequent formation of DNA single strand gaps and their recombinational repair. This high level of homologous recombination renders the proteins that resolve Holliday junctions recombination intermediates essential for viability. When homologous recombination is blocked at early steps by recFOR or recA inactivation, exonuclease V-mediated DNA degradation is required for full viability of priA mutants, indicating that unrepaired gaps are broken and that DNA degradation of the broken DNA allows the formation of viable cells. Models for the formation of single strand DNA gaps consequently to a replication restart defect and for gap processing are proposed.
journal_name
Mol Microbioljournal_title
Molecular microbiologyauthors
Grompone G,Sanchez N,Dusko Ehrlich S,Michel Bdoi
10.1111/j.1365-2958.2004.03997.xsubject
Has Abstractpub_date
2004-04-01 00:00:00pages
551-62issue
2eissn
0950-382Xissn
1365-2958pii
MMI3997journal_volume
52pub_type
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