RecA protein filaments: end-dependent dissociation from ssDNA and stabilization by RecO and RecR proteins

Shan, Qun; Bork, Julie M.; Webb, Brian; Inman, Ross B.; Cox, Michael M.

doi:10.1006/jmbi.1996.0748

Cited by 184 publications

(150 citation statements)

References 75 publications

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“…3). The RecOR complex facilitates the binding of RecA protein to SSB-coated DNA (Umezu & Kolodner 1994), and prevents the end-dependent disassembly of the RecA filament (Shan et al 1997). The RecFR complex binds primarily to double-stranded DNA and can prevent excessive extension of the filament into the adjoining duplex DNA .…”

Section: Quantifying Step 1 Under Normal Growth Conditionsmentioning

confidence: 99%

A broadening view of recombinational DNA repair in bacteria

1998

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Section: Quantifying Step 1 Under Normal Growth Conditionsmentioning

confidence: 99%

A broadening view of recombinational DNA repair in bacteria

1998

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“…In the absence of any of these genes, UV-irradiated cells fail to recover DNA synthesis following arrest, gaps persist in the DNA synthesized postirradiation, and the nascent DNA at the replication fork is extensively degraded (6-8, 10, 19, 38, 41, 47). In vitro, RecA, RecF, RecO, and RecR promote pairing between single-strand DNA and homologous duplex DNA (2,22,46,56,57), an activity that was originally characterized for its role in bringing together homologous strands of DNA during recombinational processes (5). Cellular assays indicate that the same enzymatic activity is also required during replication to maintain and process the homologous strands of the replication fork when the normal progression of the replication machinery is prevented (reviewed in reference 9).…”

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Nucleotide Excision Repair or Polymerase V-Mediated Lesion Bypass Can Act To Restore UV-Arrested Replication Forks in Escherichia coli

2005

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Nucleotide excision repair and translesion DNA synthesis are two processes that operate at arrested replication forks to reduce the frequency of recombination and promote cell survival following UV-induced DNA damage. While nucleotide excision repair is generally considered to be error free, translesion synthesis can result in mutations, making it important to identify the order and conditions that determine when each process is recruited to the arrested fork. We show here that at early times following UV irradiation, the recovery of DNA synthesis occurs through nucleotide excision repair of the lesion. In the absence of repair or when the repair capacity of the cell has been exceeded, translesion synthesis by polymerase V (Pol V) allows DNA synthesis to resume and is required to protect the arrested replication fork from degradation. Pol II and Pol IV do not contribute detectably to survival, mutagenesis, or restoration of DNA synthesis, suggesting that, in vivo, these polymerases are not functionally redundant with Pol V at UV-induced lesions. We discuss a model in which cells first use DNA repair to process replication-arresting UV lesions before resorting to mutagenic pathways such as translesion DNA synthesis to bypass these impediments to replication progression.Irradiation of cells with 254-nm UV light induces lesions that block DNA polymerases. Lesions that block polymerases are thought to either arrest the progress of the replication machinery or produce nascent-strand gaps depending on which template strand contains the lesion (3,4,17,32,45,50,53,54). Several studies using plasmid substrates indicate that lesions in the leading-strand template arrest the overall progression of the replication fork, with the nascent lagging strand continuing a short distance beyond the arrested leading strand (17,30,50,53). In contrast, lesions in the lagging-strand template are thought to generate gaps in the nascent DNA strand at sites opposite to the lesion, presumably because discontinuous synthesis of the lagging strand allows the blocked polymerase to reinitiate downstream of the lesion site (17,30,50). Events that are consistent with this can also be seen on the chromosome of UV-irradiated Escherichia coli. Following a moderate dose of UV irradiation, the rate of DNA synthesis is transiently inhibited before it efficiently recovers at a time that correlates with lesion removal (8,45). During this period of inhibition, some limited DNA synthesis is still observed that contains gaps, consistent with replication continuing past a subset of the lesions in the template (13,42,43). The repair and restoration of the DNA template in each of these two situations may involve unique enzymatic pathways and are likely to have different consequences for the cell with respect to survival and mutagenesis.Lesions that arrest the overall progression of the replication machinery would be expected to prevent the replication of the genome and are likely to result in cell lethality if the block to replication cannot be overcome. The a...

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“…Similar reactions can be catalyzed by unwinding the end using RecQ helicase coupled with strand removal by the RecJ 59-39 exonuclease (Courcelle et al 2001;Amundsen and Smith 2003). RecA can be loaded directly onto this resected ssDNA by RecBCD (Anderson andKowalczykowski 1997, 2000;Chedin and Kowalczykowski 2002;Amundsen and Smith 2003;Xu and Marians 2003) or by the RecFOR complex when the strand is coated with Single-stranded DNA binding (SSB) protein (Umezu and Kolodner 1994;Shan et al 1997;Kantake et al 2002;Ivancic-Bace et al 2003). Formation of a RecA nucleoprotein filament allows homologous pairing and strand 1 exchange between the broken end and its undamaged partner.…”

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The RuvAB Branch Migration Translocase and RecU Holliday Junction Resolvase Are Required for Double-Stranded DNA Break Repair in Bacillus subtilis

et al. 2005

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In models of Escherichia coli recombination and DNA repair, the RuvABC complex directs the branch migration and resolution of Holliday junction DNA. To probe the validity of the E. coli paradigm, we examined the impact of mutations in DruvAB and DrecU (a ruvC functional analog) on DNA repair. Under standard transformation conditions we failed to construct DruvAB DrecG, DrecU DruvAB, DrecU DrecG, or DrecU DrecJ strains. However, DruvAB could be combined with addAB (recBCD), recF, recH, DrecS, DrecQ, and DrecJ mutations. The DruvAB and DrecU mutations rendered cells extremely sensitive to DNA-damaging agents, although less sensitive than a DrecA strain. When damaged cells were analyzed, we found that RecU was recruited to defined double-stranded DNA breaks (DSBs) and colocalized with RecN. RecU localized to these centers at a later time point during DSB repair, and formation was dependent on RuvAB. In addition, expression of RecU in an E. coli ruvC mutant restored full resistance to UV light only when the ruvAB genes were present. The results demonstrate that, as with E. coli RuvABC, RuvAB targets RecU to recombination intermediates and that all three proteins are required for repair of DSBs arising from lesions in chromosomal DNA.

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RecA protein filaments: end-dependent dissociation from ssDNA and stabilization by RecO and RecR proteins

Cited by 184 publications

References 75 publications

A broadening view of recombinational DNA repair in bacteria

A broadening view of recombinational DNA repair in bacteria

Nucleotide Excision Repair or Polymerase V-Mediated Lesion Bypass Can Act To Restore UV-Arrested Replication Forks in Escherichia coli

The RuvAB Branch Migration Translocase and RecU Holliday Junction Resolvase Are Required for Double-Stranded DNA Break Repair in Bacillus subtilis

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