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http://purl.uniprot.org/citations/20472512http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20472512http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20472512http://www.w3.org/2000/01/rdf-schema#comment"In Saccharomyces cerevisiae, a DNA damage checkpoint in the S-phase is responsible for delaying DNA replication in response to genotoxic stress. This pathway is partially regulated by the checkpoint proteins Rad9, Rad17 and Rad24. Here, we describe a novel hypermutable phenotype for rad9Delta, rad17Delta and rad24Delta cells in response to a chronic 0.01% dose of the DNA alkylating agent MMS. We report that this hypermutability results from DNA damage introduction during the S-phase and is dependent on a functional translesion synthesis pathway. In addition, we performed a genetic screen for interactions with rad9Delta that confer sensitivity to 0.01% MMS. We report and quantify 25 genetic interactions with rad9Delta, many of which involve the post-replication repair machinery. From these data, we conclude that defects in S-phase checkpoint regulation lead to increased reliance on mutagenic translesion synthesis, and we describe a novel role for members of the S-phase DNA damage checkpoint in suppressing mutagenic post-replicative repair in response to sublethal MMS treatment."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.org/dc/terms/identifier"doi:10.1016/j.dnarep.2010.04.007"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.org/dc/terms/identifier"doi:10.1016/j.dnarep.2010.04.007"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Huang D."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Huang D."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Bangur C."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Bangur C."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Murakami-Sekimata A."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Murakami-Sekimata A."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Paulovich A.G."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Paulovich A.G."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Piening B.D."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/author"Piening B.D."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/name"DNA Repair"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/name"DNA Repair"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/pages"824-834"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/pages"824-834"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/title"The Saccharomyces cerevisiae RAD9, RAD17 and RAD24 genes are required for suppression of mutagenic post-replicative repair during chronic DNA damage."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/title"The Saccharomyces cerevisiae RAD9, RAD17 and RAD24 genes are required for suppression of mutagenic post-replicative repair during chronic DNA damage."xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/20472512http://purl.uniprot.org/core/volume"9"xsd:string