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

Charlotte Blessing, Katja Apelt, Diana Heuvel, Claudia Gonzalez-Leal, Magdalena B. Rother, Melanie Woude, Román González-Prieto, Adi Yifrach, Avital Parnas, Rashmi G. Shah, Tia Tyrsett Kuo, Daphne E. C. Boer, Jin Cai, Angela Kragten, Hyun-Suk Kim, Orlando D. Schärer, Alfred C. O. Vertegaal, Girish M. Shah, Sheera Adar, Hannes Lans, Haico Attikum, Andreas G. Ladurner () and Martijn S. Luijsterburg ()
Additional contact information
Charlotte Blessing: Faculty of Medicine, LMU Munich
Katja Apelt: Leiden University Medical Center (LUMC)
Diana Heuvel: Leiden University Medical Center (LUMC)
Claudia Gonzalez-Leal: Faculty of Medicine, LMU Munich
Magdalena B. Rother: Leiden University Medical Center (LUMC)
Melanie Woude: Erasmus University Medical Center
Román González-Prieto: Leiden University Medical Center (LUMC)
Adi Yifrach: The Hebrew University of Jerusalem
Avital Parnas: The Hebrew University of Jerusalem
Rashmi G. Shah: CHU-Q: Laval University Hospital Research Centre of Quebec (CHUL site)
Tia Tyrsett Kuo: Faculty of Medicine, LMU Munich
Daphne E. C. Boer: Leiden University Medical Center (LUMC)
Jin Cai: Faculty of Medicine, LMU Munich
Angela Kragten: Leiden University Medical Center (LUMC)
Hyun-Suk Kim: Institute for Basic Science
Orlando D. Schärer: Institute for Basic Science
Alfred C. O. Vertegaal: Leiden University Medical Center (LUMC)
Girish M. Shah: CHU-Q: Laval University Hospital Research Centre of Quebec (CHUL site)
Sheera Adar: The Hebrew University of Jerusalem
Hannes Lans: Erasmus University Medical Center
Haico Attikum: Leiden University Medical Center (LUMC)
Andreas G. Ladurner: Faculty of Medicine, LMU Munich
Martijn S. Luijsterburg: Leiden University Medical Center (LUMC)

Nature Communications, 2022, vol. 13, issue 1, 1-18

Abstract: 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.

Date: 2022
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DOI: 10.1038/s41467-022-31820-4

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