%0 Journal Article
%A Blessing, Charlotte
%A Apelt, Katja
%A van den Heuvel, Diana
%A Gonzalez-Leal, Claudia
%A Rother, Magdalena B
%A van der Woude, Melanie
%A González-Prieto, Román
%A Yifrach, Adi
%A Parnas, Avital
%A Shah, Rashmi G
%A Kuo, Tia Tyrsett
%A Boer, Daphne E C
%A Cai, Jin
%A Kragten, Angela
%A Kim, Hyun-Suk
%A Schärer, Orlando D
%A Vertegaal, Alfred C O
%A Shah, Girish M
%A Adar, Sheera
%A Lans, Hannes
%A van Attikum, Haico
%A Ladurner, Andreas G
%A Luijsterburg, Martijn S
%T XPC-PARP complexes engage the chromatin remodeler ALC1 to catalyze global genome DNA damage repair.
%D 2022
%U http://hdl.handle.net/10668/19540
%X 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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