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Protection of the C. elegans germ cell genome depends on diverse DNA repair pathways during normal proliferation

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dc.contributor.authorMeier, Bettina-
dc.contributor.authorVolkova, Nadezda V.-
dc.contributor.authorHong, Ye-
dc.contributor.authorBertolini, Simone-
dc.contributor.authorGonzález-Huici, Víctor-
dc.contributor.authorPetrova, Tsvetana-
dc.contributor.authorBoulton, Simon-
dc.contributor.authorCampbell, Peter J.-
dc.contributor.authorGerstung, Moritz-
dc.contributor.authorAnton Gartner-
dc.date.accessioned2021-06-09T05:30:01Z-
dc.date.accessioned2021-06-09T05:30:01Z-
dc.date.available2021-06-09T05:30:01Z-
dc.date.available2021-06-09T05:30:01Z-
dc.date.created2021-05-27-
dc.date.issued2021-04-27-
dc.identifier.issn1932-6203-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/9743-
dc.description.abstractMaintaining genome integrity is particularly important in germ cells to ensure faithful transmission of genetic information across generations. Here we systematically describe germ cell mutagenesis in wild-type and 61 DNA repair mutants cultivated over multiple generations. ~44% of the DNA repair mutants analysed showed a >2-fold increased mutagenesis with a broad spectrum of mutational outcomes. Nucleotide excision repair deficiency led to higher base substitution rates, whereas polh-1(Polη) and rev-3(Polζ) translesion synthesis polymerase mutants resulted in 50-400 bp deletions. Signatures associated with defective homologous recombination fall into two classes: 1) brc-1/BRCA1 and rad-51/RAD51 paralog mutants showed increased mutations across all mutation classes, 2) mus-81/MUS81 and slx-1/SLX1 nuclease, and him-6/BLM, helq-1/HELQ or rtel-1/RTEL1 helicase mutants primarily accumulated structural variants. Repetitive and G-quadruplex sequence-containing loci were more frequently mutated in specific DNA repair backgrounds. Tandem duplications embedded in inverted repeats were observed in helq-1 helicase mutants, and a unique pattern of 'translocations' involving homeologous sequences occurred in rip-1 recombination mutants. atm-1/ATM checkpoint mutants harboured structural variants specifically enriched in subtelomeric regions. Interestingly, locally clustered mutagenesis was only observed for combined brc-1 and cep-1/p53 deficiency. Our study provides a global view of how different DNA repair pathways contribute to prevent germ cell mutagenesis.-
dc.language영어-
dc.publisherNLM (Medline)-
dc.titleProtection of the C. elegans germ cell genome depends on diverse DNA repair pathways during normal proliferation-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000665456800015-
dc.identifier.scopusid2-s2.0-85105051985-
dc.identifier.rimsid75671-
dc.contributor.affiliatedAuthorAnton Gartner-
dc.identifier.doi10.1371/journal.pone.0250291-
dc.identifier.bibliographicCitationPLOS ONE, v.16, no.4-
dc.relation.isPartOfPLOS ONE-
dc.citation.titlePLOS ONE-
dc.citation.volume16-
dc.citation.number4-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaScience & Technology - Other Topics-
dc.relation.journalWebOfScienceCategoryMultidisciplinary Sciences-
dc.subject.keywordPlusCROSS-LINK REPAIR-
dc.subject.keywordPlusMUTATIONAL SIGNATURES-
dc.subject.keywordPlusTELOMERE MAINTENANCE-
dc.subject.keywordPlusDAMAGE RESPONSE-
dc.subject.keywordPlusCLUSTERED MUTATIONS-
dc.subject.keywordPlusPOLYMERASE-ZETA-
dc.subject.keywordPlusFANCONI-ANEMIA-
dc.subject.keywordPlusRECOMBINATION-
dc.subject.keywordPlusSTABILITY-
dc.subject.keywordPlusHELICASE-
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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