dc.creator | Blessing, Charlotte | es |
dc.creator | Apelt, Katja | es |
dc.creator | Van Den Heuvel, Diana | es |
dc.creator | González Leal, Claudia | es |
dc.creator | Rother, Magdalena B | es |
dc.creator | Van Der Woude, Melanie | es |
dc.creator | González Prieto, Román | es |
dc.creator | Luijsterburg, Martijn S. | es |
dc.date.accessioned | 2023-05-05T17:25:30Z | |
dc.date.available | 2023-05-05T17:25:30Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Blessing, C., Apelt, K., Van Den Heuvel, D., González Leal, C., Rother, M.B., Van Der Woude, M.,...,Luijsterburg, M.S. (2022). XPC–PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair. Nature Communications, 13 (1). https://doi.org/10.1038/s41467-022-31820-4. | |
dc.identifier.issn | 2041-1723 | es |
dc.identifier.uri | https://hdl.handle.net/11441/145506 | |
dc.description.abstract | Cells employ global genome nucleotide excision repair (GGR) to eliminate a broad spectrum of DNA lesions, including those induced by UV light. The lesion-recognition factor XPC initiates repair of helix-destabilizing DNA lesions, but binds poorly to lesions such as CPDs that do not destabilize DNA. How difficult-to-repair lesions are detected in chromatin is unknown. Here, we identify the poly-(ADP-ribose) polymerases PARP1 and PARP2 as constitutive interactors of XPC. Their interaction results in the XPC-stimulated synthesis of poly-(ADP-ribose) (PAR) by PARP1 at UV lesions, which in turn enables the recruitment and activation of the PAR-regulated chromatin remodeler ALC1. PARP2, on the other hand, modulates the retention of ALC1 at DNA damage sites. Notably, ALC1 mediates chromatin expansion at UV-induced DNA lesions, leading to the timely clearing of CPD lesions. Thus, we reveal how chromatin containing difficult-to-repair DNA lesions is primed for repair, providing insight into mechanisms of chromatin plasticity during GGR. | es |
dc.description.sponsorship | German Research Foundation 213249687 - SFB 1064, 325871075 - SFB 1309 | es |
dc.description.sponsorship | Dutch Cancer Society KWF-YIG 11367 | es |
dc.description.sponsorship | European Research Council 310913 | es |
dc.description.sponsorship | Netherlands Organization for Scientific Research 711.018.007 | es |
dc.description.sponsorship | Institute of Basic Science IBS-R022-A1 | es |
dc.description.sponsorship | Natural Sciences and Engineering Research Council of Canada RGPIN-2016-05868, RGPAS-492875-2016 | es |
dc.description.sponsorship | Israel Cancer Research Fund Research Career Development Award 3013004741 | es |
dc.description.sponsorship | Dutch Research Council ENW-M (OCENW.KLEIN.090), ALW.016.161.320, VI.C.182.052 | es |
dc.description.sponsorship | National Cancer Insitute P01- CA092584 | es |
dc.description.sponsorship | Israel Cancer Association 20210078 | es |
dc.description.sponsorship | Israel Science Foundation 1710/17 | es |
dc.format | application/pdf | es |
dc.format.extent | 18 p. | es |
dc.language.iso | eng | es |
dc.publisher | Springer Nature | es |
dc.relation.ispartof | Nature Communications, 13 (1). | |
dc.rights | Atribución 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | * |
dc.title | XPC–PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Biología Celular | es |
dc.relation.projectID | 213249687 - SFB 1064 | es |
dc.relation.projectID | 325871075 - SFB 1309 | es |
dc.relation.projectID | KWF-YIG 11367 | es |
dc.relation.projectID | 310913 | es |
dc.relation.projectID | 711.018.007 | es |
dc.relation.projectID | IBS-R022-A1 | es |
dc.relation.projectID | RGPIN-2016-05868 | es |
dc.relation.projectID | RGPAS-492875-2016 | es |
dc.relation.projectID | 3013004741 | es |
dc.relation.projectID | ENW-M (OCENW.KLEIN.090) | es |
dc.relation.projectID | ALW.016.161.320 | es |
dc.relation.projectID | VI.C.182.052 | es |
dc.relation.projectID | P01- CA092584 | es |
dc.relation.projectID | 20210078 | es |
dc.relation.projectID | 1710/17 | es |
dc.relation.publisherversion | https://doi.org/10.1038/s41467-022-31820-4 | es |
dc.identifier.doi | 10.1038/s41467-022-31820-4 | es |
dc.journaltitle | Nature Communications | es |
dc.publication.volumen | 13 | es |
dc.publication.issue | 1 | es |
dc.contributor.funder | Deutsche Forschungsgemeinschaft / German Research Foundation (DFG) | es |
dc.contributor.funder | Dutch Cancer Society | es |
dc.contributor.funder | European Research Council (ERC) | es |
dc.contributor.funder | Netherlands Organization for Scientific Research | es |
dc.contributor.funder | Institute of Basic Science (IBS). Korea | es |
dc.contributor.funder | Natural Sciences and Engineering Research Council of Canada (NSERC) | es |
dc.contributor.funder | Israel Cancer Research Fund Research Career Development Award | es |
dc.contributor.funder | Israel Cancer Association | es |
dc.contributor.funder | Israel Science Foundation | es |
dc.contributor.funder | Dutch Research Council | es |
dc.contributor.funder | National Cancer Institute (USA) | es |