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유전체항상성연구단
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Microhomology-mediated end joining induces hypermutagenesis at breakpoint junctions

DC Field Value Language
dc.contributor.authorSinha S.-
dc.contributor.authorLi F.-
dc.contributor.authorVillarreal D.-
dc.contributor.authorShim J.H.-
dc.contributor.authorYoon S.-
dc.contributor.authorKyungjae Myung-
dc.contributor.authorShim E.Y.-
dc.contributor.authorLee S.E.-
dc.date.accessioned2018-01-08T05:16:52Z-
dc.date.available2018-01-08T05:16:52Z-
dc.date.created2017-05-19-
dc.date.issued2017-04-
dc.identifier.issn1553-7404-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/4178-
dc.description.abstractMicrohomology (MH) flanking a DNA double-strand break (DSB) drives chromosomal rearrangements but its role in mutagenesis has not yet been analyzed. Here we determined the mutation frequency of a URA3 reporter gene placed at multiple locations distal to a DSB, which is flanked by different sizes (15-, 18-, or 203-bp) of direct repeat sequences for efficient repair in budding yeast. Induction of a DSB accumulates mutations in the reporter gene situated up to 14-kb distal to the 15-bp MH, but more modestly to those carrying 18- and 203-bp or no homology. Increased mutagenesis in MH-mediated end joining (MMEJ) appears coupled to its slower repair kinetics and the extensive resection occurring at flanking DNA. Chromosomal translocations via MMEJ also elevate mutagenesis of the flanking DNA sequences 7.1 kb distal to the breakpoint junction as compared to those without MH. The results suggest that MMEJ could destabilize genomes by triggering structural alterations and increasing mutation burden. © 2017 Sinha et al-
dc.description.uri1-
dc.language영어-
dc.publisherPUBLIC LIBRARY SCIENCE-
dc.titleMicrohomology-mediated end joining induces hypermutagenesis at breakpoint junctions-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000402549200028-
dc.identifier.scopusid2-s2.0-85018440543-
dc.identifier.rimsid59510-
dc.date.tcdate2018-10-01-
dc.contributor.affiliatedAuthorKyungjae Myung-
dc.identifier.doi10.1371/journal.pgen.1006714-
dc.identifier.bibliographicCitationPLOS GENETICS, v.13, no.4, pp.e1006714-
dc.citation.titlePLOS GENETICS-
dc.citation.volume13-
dc.citation.number4-
dc.citation.startPagee1006714-
dc.date.scptcdate2018-10-01-
dc.description.wostc9-
dc.description.scptc9-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusDOUBLE-STRAND BREAKS-
dc.subject.keywordPlusREPAIR PATHWAY CHOICE-
dc.subject.keywordPlusSACCHAROMYCES-CEREVISIAE-
dc.subject.keywordPlusDNA-SYNTHESIS-
dc.subject.keywordPlusHOMOLOGOUS RECOMBINATION-
dc.subject.keywordPlusREPLICATIVE MECHANISMS-
dc.subject.keywordPlusCELL-CYCLE-
dc.subject.keywordPlusRESECTION-
dc.subject.keywordPlusPOLYMERASES-
dc.subject.keywordPlusMUTATIONS-
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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