Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S-phase but arrest permanently in G2 after cisplatin treatment

Grossmann, Kenneth F.; Ward, Alex M.; Moses, Robb E.

doi:10.1016/s0921-8777(00)00035-5

Cited by 38 publications

(30 citation statements)

References 40 publications

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“…The epistatic relationship between PSO2 and a variety of NER genes reported here and elsewhere (now including rad1, rad2, rad3, and rad4) suggests that these factors contribute to a common repair pathway (28). There is a clear ICL incision defect in NER mutants, not observed in pso2 mutants, placing Pso2 downstream of the incision step of NER (27,39,45,71). As first reported in references 39 and 71, and substantiated here, pso2 mutants fail to repair the DSBs produced at ICLs.…”

Section: Discussionsupporting

confidence: 79%

“…Following exposure to 8-methoxypsoralen-UVA, cisplatin, and nitrogen mustard, a complete abolition of cross-link incision events was observed in NER-defective strains (30,39,47,71). In contrast, pso2 cells incised the cross-links normally, and both single-and double-strand break intermediates were formed (27,39,71). However, these were not subsequently reconstituted to intact double-stranded DNA (35,39,71).…”

mentioning

confidence: 99%

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DNA Interstrand Cross-Link Repair in theSaccharomyces cerevisiaeCell Cycle: Overlapping Roles forPSO2(SNM1) with MutS Factors andEXO1during S Phase

Barber

Ward

Hartley

et al. 2005

Molecular and Cellular Biology

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Pso2/Snm1 is a member of the ␤-CASP metallo-␤-lactamase family of proteins that include the V(D)J recombination factor Artemis. Saccharomyces cerevisiae pso2 mutants are specifically sensitive to agents that induce DNA interstrand cross-links (ICLs). Here we establish a novel overlapping function for PSO2 with MutS mismatch repair factors and the 5-3 exonuclease Exo1 in the repair of DNA ICLs, which is confined to S phase. Our data demonstrate a requirement for NER and Pso2, or Exo1 and MutS factors, in the processing of ICLs, and this is required prior to the repair of ICL-induced DNA double-strand breaks (DSBs) that form during replication. Using a chromosomally integrated inverted-repeat substrate, we also show that loss of both pso2 and exo1/msh2 reduces spontaneous homologous recombination rates. Therefore, PSO2, EXO1, and MSH2 also appear to have overlapping roles in the processing of some forms of endogenous DNA damage that occur at an irreversibly collapsed replication fork. Significantly, our analysis of ICL repair in cells synchronized for each cell cycle phase has revealed that homologous recombination does not play a major role in the direct repair of ICLs, even in G 2 , when a suitable template is readily available. Rather, we propose that recombination is primarily involved in the repair of DSBs that arise from the collapse of replication forks at ICLs. These findings have led to considerable clarification of the complex genetic relationship between various ICL repair pathways.

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

DNA Interstrand Cross-Link Repair in theSaccharomyces cerevisiaeCell Cycle: Overlapping Roles forPSO2(SNM1) with MutS Factors andEXO1during S Phase

Barber

Ward

Hartley

et al. 2005

Molecular and Cellular Biology

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“…On the other hand, the yeast rev3 mutant is sensitive to cisplatin and 8-methoxysporalen (Grossmann et al, 2000), which, like MMC, cause interstrand cross-links (ICLs) in double-stranded DNA. Because ICL prevents DNA strand separation, the DNA cannot be repaired by the usual excision repair pathway.…”

Section: Atrev3 Is Essential For the Tolerance Of Dna Damagementioning

confidence: 99%

“…However, one possibility is that ICLs require some specific DNA-repair process that involves REV3. Grossmann et al (2000) proposed an ICL repair pathway in which ICLs are excised by an NER and then the resultant double-strand break is repaired by the recombination repair pathway or by the nonhomologous end-joining pathway. In addition, Holbeck and Strathern (1997) reported that in yeast, the high mutation frequency induced in the repair process of double-strand breaks was abolished by elimination of the REV3 gene.…”

Section: Atrev3 Is Essential For the Tolerance Of Dna Damagementioning

confidence: 99%

Disruption of theAtREV3Gene Causes Hypersensitivity to Ultraviolet B Light and γ-Rays in Arabidopsis: Implication of the Presence of a Translesion Synthesis Mechanism in Plants [W]

Sakamoto¹,

Lan

Hase³

et al. 2003

The Plant Cell

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To investigate UV light response mechanisms in higher plants, we isolated a UV light-sensitive mutant, rev3-1 , in Arabidopsis. The root growth of rev3-1 was inhibited after UV-B irradiation under both light and dark conditions. We found that chromosome 1 of rev3-1 was broken at a minimum of three points, causing chromosome inversion and translocation. A gene disrupted by this rearrangement encoded the catalytic subunit of DNA polymerase ( AtREV3 ), which is thought to be involved in translesion synthesis. The rev3-1 seedlings also were sensitive to ␥ -rays and mitomycin C, which are known to inhibit DNA replication. Incorporation of bromodeoxyuridine after UV-B irradiation was less in rev3-1 than in the wild type. These results indicate that UV light-damaged DNA interrupted DNA replication in the rev3-1 mutant, leading to the inhibition of cell division and root elongation.

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“…A second round of NER action removes the remaining monoadduct. In yeast, a third poorly understood pathway involving SNM1 may also be present [8,9].…”

Section: Introductionmentioning

confidence: 99%

Double-strand breaks induce homologous recombinational repair of interstrand cross-links via cooperation of MSH2, ERCC1-XPF, REV3, and the Fanconi anemia pathway

Zhang

Liu

et al. 2007

DNA Repair

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DNA interstrand cross-linking agents have been widely used in chemotherapeutic treatment of cancer. The majority of interstrand cross-links (ICLs) in mammalian cells are removed via a complex process that involves the formation of double strand breaks at replication forks, incision of the ICL, and subsequent error-free repair by homologous recombination. How double strand breaks effect the removal of ICLs and the downstream homologous recombination process is not clear. Here, we describe a plasmid-based recombination assay in which one copy of the CFP gene is inactivated by a site-specific psoralen ICL and can be repaired by gene conversion with a mutated homologous donor sequence. We found that the homology dependent recombination (HDR) is inhibited by the ICL. However, when we introduced a double strand break adjacent to the site of the ICL, the removal of the ICL was enhanced and the substrate was funneled into a HDR repair pathway. This process was not dependent on the nucleotide excision repair pathway, but did require the ERCC1-XPF endonuclease and REV3. In addition, both the Fanconi anemia pathway and the mismatch repair protein MSH2 were required for the recombinational repair processing of the ICL. These results suggest that the juxtaposition of an ICL and a DSB stimulates repair of ICLs through a process requiring components of mismatch repair, ERCC1-XPF, REV3, Fanconi anemia proteins, and homologous recombination repair factors.

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Saccharomyces cerevisiae lacking Snm1, Rev3 or Rad51 have a normal S-phase but arrest permanently in G2 after cisplatin treatment

Cited by 38 publications

References 40 publications

DNA Interstrand Cross-Link Repair in theSaccharomyces cerevisiaeCell Cycle: Overlapping Roles forPSO2(SNM1) with MutS Factors andEXO1during S Phase

DNA Interstrand Cross-Link Repair in theSaccharomyces cerevisiaeCell Cycle: Overlapping Roles forPSO2(SNM1) with MutS Factors andEXO1during S Phase

Disruption of theAtREV3Gene Causes Hypersensitivity to Ultraviolet B Light and γ-Rays in Arabidopsis: Implication of the Presence of a Translesion Synthesis Mechanism in Plants [W]

Double-strand breaks induce homologous recombinational repair of interstrand cross-links via cooperation of MSH2, ERCC1-XPF, REV3, and the Fanconi anemia pathway

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