Published May 5, 2023 | Version v1
Publication

XPC–PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair

Description

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.

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German Research Foundation 213249687 - SFB 1064, 325871075 - SFB 1309

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Dutch Cancer Society KWF-YIG 11367

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European Research Council 310913

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Netherlands Organization for Scientific Research 711.018.007

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Institute of Basic Science IBS-R022-A1

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Natural Sciences and Engineering Research Council of Canada RGPIN-2016-05868, RGPAS-492875-2016

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Israel Cancer Research Fund Research Career Development Award 3013004741

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Dutch Research Council ENW-M (OCENW.KLEIN.090), ALW.016.161.320, VI.C.182.052

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National Cancer Insitute P01- CA092584

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Israel Cancer Association 20210078

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Israel Science Foundation 1710/17

Additional details

Identifiers

URL
https://idus.us.es/handle//11441/145506
URN
urn:oai:idus.us.es:11441/145506

Origin repository

Origin repository
USE