Sökning: onr:"swepub:oai:DiVA.org:su-183975" > MutS alpha deficien...
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000 | 03260naa a2200385 4500 | |
001 | oai:DiVA.org:su-183975 | |
003 | SwePub | |
008 | 200924s2020 | |||||||||||000 ||eng| | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-1839752 URI |
024 | 7 | a https://doi.org/10.1016/j.dnarep.2020.1028702 DOI |
040 | a (SwePub)su | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Berg, Ingrid L.u Stockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut4 aut0 (Swepub:su)berg |
245 | 1 0 | a MutS alpha deficiency increases tolerance to DNA damage in yeast lacking postreplication repair |
264 | 1 | b Elsevier BV,c 2020 |
338 | a print2 rdacarrier | |
520 | a By combining mutations in DNA repair genes, important and unexpected interactions between different repair pathways can be discovered. In this study, we identified a novel link between mismatch repair (MMR) genes and postreplication repair (PRR) in Saccharomyces cerevisiae. Strains lacking Rad5 (HLTF in mammals), a protein important for restarting stalled replication forks in the error-free PRR pathway, were supersensitive to the DNA methylating agent methyl methanesulfonate (MMS). Deletion of the mismatch repair genes, MSH2 or MSH6, which together constitutes the MutS alpha complex, partially suppressed the MMS super-sensitivity of the rad5 Delta, strain. Deletion of MSH2 also suppressed the MMS sensitivity of mms2 Delta, which acts together with Rad5 in error-free PRR. However, inactivating the mismatch repair genes MSH3 and MLH1 did not suppress rad5 Delta, showing that the suppression was specific for disabling MutS alpha. The partial suppression did not require translesion DNA synthesis (REV1, REV3 or RAD30), base excision repair (MAGI) or homologous recombination (RAD51). Instead, the underlying mechanism was dependent on RAD52 while independent of established pathways involving RAD52, like single-strand annealing and break-induced replication. We propose a Rad5- and Rad51-independent template switch pathway, capable of compensating for the loss of the error-free template-switch subpathway of postreplication repair, triggered by the loss of MutS alpha. | |
650 | 7 | a NATURVETENSKAPx Biologi0 (SwePub)1062 hsv//swe |
650 | 7 | a NATURAL SCIENCESx Biological Sciences0 (SwePub)1062 hsv//eng |
653 | a DNA damage tolerance | |
653 | a Postreplication repair | |
653 | a Template switch | |
653 | a Rad5 | |
653 | a Msh2 | |
700 | 1 | a Persson, Jan-Olovu Stockholms universitet,Matematiska institutionen4 aut0 (Swepub:su)japer |
700 | 1 | a Åström, Stefan U.u Stockholms universitet,Institutionen för molekylär biovetenskap, Wenner-Grens institut4 aut0 (Swepub:su)stast |
710 | 2 | a Stockholms universitetb Institutionen för molekylär biovetenskap, Wenner-Grens institut4 org |
773 | 0 | t DNA Repaird : Elsevier BVg 91-92q 91-92x 1568-7864x 1568-7856 |
856 | 4 | u https://doi.org/10.1016/j.dnarep.2020.102870y Fulltext |
856 | 4 | u https://doi.org/10.1016/j.dnarep.2020.102870 |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-183975 |
856 | 4 8 | u https://doi.org/10.1016/j.dnarep.2020.102870 |
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