Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-9181
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dc.contributor.authorSchindler, Natalie-
dc.contributor.authorTonn, Matthias-
dc.contributor.authorKellner, Vanessa-
dc.contributor.authorFung, Jia Jun-
dc.contributor.authorLockhart, Arianna-
dc.contributor.authorVydzhak, Olga-
dc.contributor.authorJuretschke, Thomas-
dc.contributor.authorMöckel, Stefanie-
dc.contributor.authorBeli, Petra-
dc.contributor.authorKhmelinskii, Anton-
dc.contributor.authorLuke, Brian-
dc.date.accessioned2023-06-15T11:53:52Z-
dc.date.available2023-06-15T11:53:52Z-
dc.date.issued2023-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/9198-
dc.description.abstractSingle ribonucleoside monophosphates (rNMPs) are transiently present in eukaryotic genomes. The RNase H2-dependent ribonucleotide excision repair (RER) pathway ensures error-free rNMP removal. In some pathological conditions, rNMP removal is impaired. If these rNMPs hydrolyze during, or prior to, S phase, toxic single-ended double-strand breaks (seDSBs) can occur upon an encounter with replication forks. How such rNMP-derived seDSB lesions are repaired is unclear. We expressed a cell cycle phase restricted allele of RNase H2 to nick at rNMPs in S phase and study their repair. Although Top1 is dispensable, the RAD52 epistasis group and Rtt101Mms1-Mms22 dependent ubiquitylation of histone H3 become essential for rNMP-derived lesion tolerance. Consistently, loss of Rtt101Mms1-Mms22 combined with RNase H2 dysfunction leads to compromised cellular fitness. We refer to this repair pathway as nick lesion repair (NLR). The NLR genetic network may have important implications in the context of human pathologies.en_GB
dc.description.sponsorshipDeutsche Forschungsgemeinschaft (DFG)|491381577|Open-Access-Publikationskosten 2022–2024 Universität Mainz - Universitätsmedizin-
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc570 Biowissenschaftende_DE
dc.subject.ddc570 Life sciencesen_GB
dc.titleGenetic requirements for repair of lesions caused by single genomic ribonucleotides in S phaseen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-9181-
jgu.type.contenttypeScientific articlede
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 10 Biologiede
jgu.organisation.number7970-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleNature Communicationsde
jgu.journal.volume14de
jgu.pages.alternative1227de
jgu.publisher.year2023-
jgu.publisher.nameSpringer Naturede
jgu.publisher.placeLondonde
jgu.publisher.issn2041-1723de
jgu.organisation.placeMainz-
jgu.subject.ddccode570de
jgu.publisher.doi10.1038/s41467-023-36866-6de
jgu.organisation.rorhttps://ror.org/023b0x485-
jgu.subject.dfgLebenswissenschaftende
Appears in collections:DFG-491381577-G

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