Repair of exogenous (plasmid) DNA damaged by photoaddition of 8-methoxypsoralen in the yeast Saccharomyces cerevisiae

Magaña‐Schwencke, Nieve; Averbeck, D.

doi:10.1016/0027-5107(91)90222-a

Cited by 15 publications

(5 citation statements)

References 32 publications

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“…Repair may also occur via the translesion repair pathway, involving RAD6 and RAD18 (51). Yeast translesion repair pathway mutants are not defective in the repair of an ICL on a plasmid, in contrast to recombination repair pathway mutants, suggesting that chromatin structure can have an important influence (39). On the other hand, rad52 mutants, which are impaired in recombination repair, are hardly sensitive to nitrogen mustard, suggesting that the repair pathway used may depend on the ICL agent (51).…”

Section: Discussionmentioning

confidence: 99%

“…S. cerevisiae snm1 cells show synergism with mutants from both the translesion and the recombination repair pathways with regard to sensitivity to ICL agents, suggesting that Snm1 functions in an alternative pathway (24,51). Moreover, snm1 cells are capable of repairing an ICL on a plasmid, suggesting that the activity of Snm1 may be related to the modulation of chromosomal structure (39). The sensitivity of snm1 mutants to all ICL agents tested suggests that Snm1 is involved in an ICL agent-independent step and therefore probably after the formation of ICLs (6,25,49).…”

Section: Discussionmentioning

confidence: 99%

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Disruption of Mouse SNM1 Causes Increased Sensitivity to the DNA Interstrand Cross-Linking Agent Mitomycin C

Dronkert

Wit

Boeve

et al. 2000

Molecular and Cellular Biology

118

110

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DNA interstrand cross-links (ICLs) represent lethal DNA damage, because they block transcription, replication, and segregation of DNA. Because of their genotoxicity, agents inducing ICLs are often used in antitumor therapy. The repair of ICLs is complex and involves proteins belonging to nucleotide excision, recombination, and translesion DNA repair pathways in Escherichia coli, Saccharomyces cerevisiae, and mammals. We cloned and analyzed mammalian homologs of the S. cerevisiae gene SNM1 (PSO2), which is specifically involved in ICL repair. Human Snm1, a nuclear protein, was ubiquitously expressed at a very low level. We generated mouse SNM1 ؊/؊ embryonic stem cells and showed that these cells were sensitive to mitomycin C. In contrast to S. cerevisiae snm1 mutants, they were not significantly sensitive to other ICL agents, probably due to redundancy in mammalian ICL repair and the existence of other SNM1 homologs. The sensitivity to mitomycin C was complemented by transfection of the human SNM1 cDNA and by targeting of a genomic cDNA-murine SNM1 fusion construct to the disrupted locus. We also generated mice deficient for murine SNM1. They were viable and fertile and showed no major abnormalities. However, they were sensitive to mitomycin C. The ICL sensitivity of the mammalian SNM1 mutant suggests that SNM1 function and, by implication, ICL repair are at least partially conserved between S. cerevisiae and mammals.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Disruption of Mouse SNM1 Causes Increased Sensitivity to the DNA Interstrand Cross-Linking Agent Mitomycin C

Dronkert

Wit

Boeve

et al. 2000

Molecular and Cellular Biology

118

110

View full text Add to dashboard Cite

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“…Rad1p may play a role in gene conversion events in S. cerevisae through an interaction with Msh2p (Studamire et al ., 1999). Rad1p has also been implicated in the repair of exogenous DNA (Magana‐Schwencke and Averbeck, 1991) and may be recruited to sites of DNA damage through interaction, again, with Msh2p (Nicholson et al ., 2000). But perhaps the most relevant activity of Rad1p is that its involvement in the repair of base–base mismatches present in recombination intermediates (Kirkpatrick et al ., 1997; Nicholson et al ., 2000).…”

Section: Discussionmentioning

confidence: 99%

In vitro and in vivo nucleotide exchange directed by chimeric RNA/DNA oligonucleotides in Saccharomyces cerevisae

Rice

Bruner

Czymmek

et al. 2001

Molecular Microbiology

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SummaryTargeted gene repair directed by chimeric RNA/DNA oligonucleotides has proven successful in eukaryotic cells including animal and plant models. In many cases, however, there has been a disparity in the levels of gene correction or frequency. While the delivery of these chimera into the nucleus and the long-term stability or purity of these molecules may contribute to this variability, understanding the molecular regulation of conversion is the key to improving or stabilizing frequency. To this end, we have identified genes that control targeted repair, using the genetically tractable organism, Saccharomyces cerevisae and a bank of yeast mutants.Results from experiments in cell-free extracts focused our attention on RAD52, RAD1 and RAD59 as central regulatory factors. RAD1 and RAD59 appear to be required for high levels of conversion whereas RAD52 appears to act, surprisingly, in a suppressive fashion. Results from the in vitro experiments were translated into targeting experiments in vivo. Here, mutations in a fusion construct, containing a marker gene, were converted to wild type, evidenced by the expression of green fluorescence in converted cells. Because the repaired fusion gene contains a corrected neomycin sequence, cells were subsequently placed under G418 selection and conversion confirmed at the genetic level. Taken together, these results establish, for the first time, genes that participate in the regulation of targeted gene repair and provide a novel system for evaluating true frequencies of correction. Importantly, this system enables visualization of corrected (green) and uncorrected (clear) cells enabling measurements of conversion in real time.

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“…Cells defective in rad6 display a pleiotropic phenotype, indicating the involvement of this factor in many cellular processes. Although Rad6 is not needed for the maintenance of 8‐MOP adducted plasmids (Magana‐Schwencke & Averbeck, 1991), the repair of 8‐MOP ICL is impaired in a rad6 strain (Chanet et al , 1985). The strain is also sensitive to CDDP, HN2 and MMC, with the sensitivity being higher than that for cells with impaired HRR (Simon et al , 2000).…”

Section: Interstrand Cross‐link Repairmentioning

confidence: 99%

“…This endonuclease activity plays a key role in ICL repair, as the absence of Rad1‐Rad10 abolishes the incisions of TMP ICL and causes high sensitivity to TMP (Miller et al , 1982b) and CDDP (Abe et al , 1994). Rad1 takes part in the repair of plasmid‐born 8‐MOP adducts (Magana‐Schwencke & Averbeck, 1991) and in the integration of plasmids carrying a single HMT ICL. Although similar transformation frequencies can be observed in rad1 and wild‐type cells (Greenberg et al , 2001; Saffran et al , 2004), half of the stable transformants obtained with plasmids cross‐linked in vitro by AMT in rad1 cells result from gene conversion events instead of cross‐overs, and this is not applicable to other NER factors examined, e.g.…”

Section: Interstrand Cross‐link Repairmentioning

confidence: 99%

DNA interstrand cross-link repair inSaccharomyces cerevisiae

2007

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DNA interstrand cross-links (ICL) present a formidable challenge to the cellular DNA repair apparatus. For Escherichia coli, a pathway which combines nucleotide excision repair (NER) and homologous recombination repair (HRR) to eliminate ICL has been characterized in detail, both genetically and biochemically. Mechanisms of ICL repair in eukaryotes have proved more difficult to define, primarily as a result of the fact that several pathways appear compete for ICL repair intermediates, and also because these competing activities are regulated in the cell cycle. The budding yeast Saccharomyces cerevisiae has proven a powerful tool for dissecting ICL repair. Important roles for NER, HRR and postreplication/translesion synthesis pathways have all been identified. Here we review, with reference to similarities and differences in higher eukaryotes, what has been discovered to date concerning ICL repair in this simple eukaryote.

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Repair of exogenous (plasmid) DNA damaged by photoaddition of 8-methoxypsoralen in the yeast Saccharomyces cerevisiae

Cited by 15 publications

References 32 publications

Disruption of Mouse SNM1 Causes Increased Sensitivity to the DNA Interstrand Cross-Linking Agent Mitomycin C

Disruption of Mouse SNM1 Causes Increased Sensitivity to the DNA Interstrand Cross-Linking Agent Mitomycin C

In vitro and in vivo nucleotide exchange directed by chimeric RNA/DNA oligonucleotides in Saccharomyces cerevisae

DNA interstrand cross-link repair inSaccharomyces cerevisiae

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