Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates
Homologous recombination is an evolutionally conserved mechanism that promotes genome stability through the faithful repair of double-strand breaks and single-strand gaps in DNA, and the recovery of stalled or collapsed replication forks. Saccharomyces cerevisiae ATP-dependent DNA helicase Srs2 (a m...
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| description | Homologous recombination is an evolutionally conserved mechanism that promotes genome stability through the faithful repair of double-strand breaks and single-strand gaps in DNA, and the recovery of stalled or collapsed replication forks. Saccharomyces cerevisiae ATP-dependent DNA helicase Srs2 (a member of the highly conserved UvrD family of helicases) has multiple roles in regulating homologous recombination. A mutation (srs2K41A) resulting in a helicase-dead mutant of Srs2 was found to be lethal in diploid, but not in haploid, cells. In diploid cells, Srs2K41A caused the accumulation of inter-homolog joint molecule intermediates, increased the levels of spontaneous Rad52 foci, and induced gross chromosomal rearrangements. Srs2K41A lethality and accumulation of joint molecules were suppressed by inactivating Rad51 or deleting the Rad51-interaction domain of Srs2, whereas phosphorylation and sumoylation of Srs2 and its interaction with sumoylated proliferating cell nuclear antigen (PCNA) were not required for lethality. The structure-specific complex of crossover junction endonucleases Mus81 and Mms4 was also required for viability of diploid, but not haploid, SRS2 deletion mutants (srs2Δ), and diploid srs2Δ mus81Δ mutants accumulated joint molecule intermediates. Our data suggest that Srs2 and Mus81-Mms4 have critical roles in preventing the formation of (or in resolving) toxic inter-homolog joint molecules, which could otherwise interfere with chromosome segregation and lead to genetic instability. |
| doi_str_mv | 10.1371/journal.pgen.1006136 |
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Saccharomyces cerevisiae ATP-dependent DNA helicase Srs2 (a member of the highly conserved UvrD family of helicases) has multiple roles in regulating homologous recombination. A mutation (srs2K41A) resulting in a helicase-dead mutant of Srs2 was found to be lethal in diploid, but not in haploid, cells. In diploid cells, Srs2K41A caused the accumulation of inter-homolog joint molecule intermediates, increased the levels of spontaneous Rad52 foci, and induced gross chromosomal rearrangements. Srs2K41A lethality and accumulation of joint molecules were suppressed by inactivating Rad51 or deleting the Rad51-interaction domain of Srs2, whereas phosphorylation and sumoylation of Srs2 and its interaction with sumoylated proliferating cell nuclear antigen (PCNA) were not required for lethality. The structure-specific complex of crossover junction endonucleases Mus81 and Mms4 was also required for viability of diploid, but not haploid, SRS2 deletion mutants (srs2Δ), and diploid srs2Δ mus81Δ mutants accumulated joint molecule intermediates. Our data suggest that Srs2 and Mus81-Mms4 have critical roles in preventing the formation of (or in resolving) toxic inter-homolog joint molecules, which could otherwise interfere with chromosome segregation and lead to genetic instability.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1006136</identifier><identifier>PMID: 27390022</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antigens ; Biology and Life Sciences ; Chromosome Segregation - genetics ; Chromosomes ; Deoxyribonucleic acid ; Diploidy ; DNA ; DNA Breaks, Double-Stranded - drug effects ; DNA damage ; DNA Helicases - genetics ; DNA Replication - genetics ; DNA-Binding Proteins - genetics ; Endonucleases - genetics ; Flap Endonucleases - genetics ; Genetic recombination ; Genomes ; Genomic Instability ; Haploidy ; Homologous Recombination - genetics ; Homology (Biology) ; Medicine and Health Sciences ; Mutation ; Observations ; Phosphorylation - genetics ; Physical Sciences ; Plasmids ; Proliferating Cell Nuclear Antigen - genetics ; Rad52 DNA Repair and Recombination Protein - genetics ; Recombination, Genetic ; Roles ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae - genetics ; Saccharomyces cerevisiae Proteins - genetics ; Sumoylation - genetics ; Yeast</subject><ispartof>PLoS genetics, 2016-07, Vol.12 (7), p.e1006136-e1006136</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Keyamura K, Arai K, Hishida T (2016) Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates. PLoS Genet 12(7): e1006136. doi:10.1371/journal.pgen.1006136</rights><rights>2016 Keyamura et al 2016 Keyamura et al</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Keyamura K, Arai K, Hishida T (2016) Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates. 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The structure-specific complex of crossover junction endonucleases Mus81 and Mms4 was also required for viability of diploid, but not haploid, SRS2 deletion mutants (srs2Δ), and diploid srs2Δ mus81Δ mutants accumulated joint molecule intermediates. Our data suggest that Srs2 and Mus81-Mms4 have critical roles in preventing the formation of (or in resolving) toxic inter-homolog joint molecules, which could otherwise interfere with chromosome segregation and lead to genetic instability.</description><subject>Antigens</subject><subject>Biology and Life Sciences</subject><subject>Chromosome Segregation - genetics</subject><subject>Chromosomes</subject><subject>Deoxyribonucleic acid</subject><subject>Diploidy</subject><subject>DNA</subject><subject>DNA Breaks, Double-Stranded - drug effects</subject><subject>DNA damage</subject><subject>DNA Helicases - genetics</subject><subject>DNA Replication - genetics</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Endonucleases - genetics</subject><subject>Flap Endonucleases - genetics</subject><subject>Genetic recombination</subject><subject>Genomes</subject><subject>Genomic Instability</subject><subject>Haploidy</subject><subject>Homologous Recombination - genetics</subject><subject>Homology (Biology)</subject><subject>Medicine and Health Sciences</subject><subject>Mutation</subject><subject>Observations</subject><subject>Phosphorylation - 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genetics</topic><topic>Chromosomes</topic><topic>Deoxyribonucleic acid</topic><topic>Diploidy</topic><topic>DNA</topic><topic>DNA Breaks, Double-Stranded - drug effects</topic><topic>DNA damage</topic><topic>DNA Helicases - genetics</topic><topic>DNA Replication - genetics</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Endonucleases - genetics</topic><topic>Flap Endonucleases - genetics</topic><topic>Genetic recombination</topic><topic>Genomes</topic><topic>Genomic Instability</topic><topic>Haploidy</topic><topic>Homologous Recombination - genetics</topic><topic>Homology (Biology)</topic><topic>Medicine and Health Sciences</topic><topic>Mutation</topic><topic>Observations</topic><topic>Phosphorylation - genetics</topic><topic>Physical Sciences</topic><topic>Plasmids</topic><topic>Proliferating Cell Nuclear Antigen - genetics</topic><topic>Rad52 DNA Repair and Recombination Protein - genetics</topic><topic>Recombination, Genetic</topic><topic>Roles</topic><topic>Saccharomyces cerevisiae</topic><topic>Saccharomyces cerevisiae - genetics</topic><topic>Saccharomyces cerevisiae Proteins - genetics</topic><topic>Sumoylation - genetics</topic><topic>Yeast</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Keyamura, Kenji</creatorcontrib><creatorcontrib>Arai, Kota</creatorcontrib><creatorcontrib>Hishida, Takashi</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Keyamura, Kenji</au><au>Arai, Kota</au><au>Hishida, Takashi</au><au>Lisby, Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2016-07-07</date><risdate>2016</risdate><volume>12</volume><issue>7</issue><spage>e1006136</spage><epage>e1006136</epage><pages>e1006136-e1006136</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>Homologous recombination is an evolutionally conserved mechanism that promotes genome stability through the faithful repair of double-strand breaks and single-strand gaps in DNA, and the recovery of stalled or collapsed replication forks. Saccharomyces cerevisiae ATP-dependent DNA helicase Srs2 (a member of the highly conserved UvrD family of helicases) has multiple roles in regulating homologous recombination. A mutation (srs2K41A) resulting in a helicase-dead mutant of Srs2 was found to be lethal in diploid, but not in haploid, cells. In diploid cells, Srs2K41A caused the accumulation of inter-homolog joint molecule intermediates, increased the levels of spontaneous Rad52 foci, and induced gross chromosomal rearrangements. Srs2K41A lethality and accumulation of joint molecules were suppressed by inactivating Rad51 or deleting the Rad51-interaction domain of Srs2, whereas phosphorylation and sumoylation of Srs2 and its interaction with sumoylated proliferating cell nuclear antigen (PCNA) were not required for lethality. The structure-specific complex of crossover junction endonucleases Mus81 and Mms4 was also required for viability of diploid, but not haploid, SRS2 deletion mutants (srs2Δ), and diploid srs2Δ mus81Δ mutants accumulated joint molecule intermediates. Our data suggest that Srs2 and Mus81-Mms4 have critical roles in preventing the formation of (or in resolving) toxic inter-homolog joint molecules, which could otherwise interfere with chromosome segregation and lead to genetic instability.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27390022</pmid><doi>10.1371/journal.pgen.1006136</doi><orcidid>https://orcid.org/0000-0002-9752-6599</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Antigens Biology and Life Sciences Chromosome Segregation - genetics Chromosomes Deoxyribonucleic acid Diploidy DNA DNA Breaks, Double-Stranded - drug effects DNA damage DNA Helicases - genetics DNA Replication - genetics DNA-Binding Proteins - genetics Endonucleases - genetics Flap Endonucleases - genetics Genetic recombination Genomes Genomic Instability Haploidy Homologous Recombination - genetics Homology (Biology) Medicine and Health Sciences Mutation Observations Phosphorylation - genetics Physical Sciences Plasmids Proliferating Cell Nuclear Antigen - genetics Rad52 DNA Repair and Recombination Protein - genetics Recombination, Genetic Roles Saccharomyces cerevisiae Saccharomyces cerevisiae - genetics Saccharomyces cerevisiae Proteins - genetics Sumoylation - genetics Yeast |
| title | Srs2 and Mus81-Mms4 Prevent Accumulation of Toxic Inter-Homolog Recombination Intermediates |
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