ArticleMolecular and cellular biology2005
DNA interstrand cross-link repair in the Saccharomyces cerevisiae cell cycle: overlapping roles for PSO2 (SNM1) with MutS factors and EXO1 during S phase.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 74 citations in OpenAlex.
- Repair of genomic interstrand crosslinks.DNA repair · 2024Review
- Dual targeting of Saccharomyces cerevisiae Pso2 to mitochondria and the nucleus, and its functional relevance in the repair of DNA interstrand crosslinks.G3 (Bethesda, Md.) · 2022Article
- Fanconi anemia-independent DNA inter-strand crosslink repair in eukaryotes.Progress in biophysics and molecular biology · 2020Review
- The roles of fission yeast exonuclease 5 in nuclear and mitochondrial genome stability.DNA repair · 2019Article
- Distinct roles of XPF-ERCC1 and Rad1-Rad10-Saw1 in replication-coupled and uncoupled inter-strand crosslink repair.Nature communications · 2018Article
- Sensing and Processing of DNA Interstrand Crosslinks by the Mismatch Repair Pathway.Cell reports · 2017Article
- SNM1B/Apollo in the DNA damage response and telomere maintenance.Oncotarget · 2017Review
- Small molecule inhibitors uncover synthetic genetic interactions of human flap endonuclease 1 (FEN1) with DNA damage response genes.PloS one · 2017Article
- Article
- The differences between ICL repair during and outside of S phase.Trends in biochemical sciences · 2013Review
- A prototypical Fanconi anemia pathway in lower eukaryotes?Cell cycle (Georgetown, Tex.) · 2012Article
- Pso2 (SNM1) is a DNA structure-specific endonuclease.Nucleic acids research · 2012Article
- Components of a Fanconi-like pathway control Pso2-independent DNA interstrand crosslink repair in yeast.PLoS genetics · 2012Article
- Human SNM1A and XPF-ERCC1 collaborate to initiate DNA interstrand cross-link repair.Genes & development · 2011Article
- The telomeric protein SNM1B/Apollo is required for normal cell proliferation and embryonic development.Aging cell · 2010Article
- Meiotic versus mitotic recombination: two different routes for double-strand break repair: the different functions of meiotic versus mitotic DSB repair are reflected in different pathway usage and different outcomes.BioEssays : news and reviews in molecular, cellular and developmental biology · 2010Review
- Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle.Environmental and molecular mutagenesis · 2010Review
- The multifunctional SNM1 gene family: not just nucleases.Future oncology (London, England) · 2010Review
- DNA interstrand crosslink repair in mammalian cells: step by step.Critical reviews in biochemistry and molecular biology · 2010Review
- Repair of laser-localized DNA interstrand cross-links in G1 phase mammalian cells.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pso2/Snm1 is a member of the beta-CASP metallo-beta-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 G2, 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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