Abstract
All cells rely on genomic stability mechanisms to protect against DNA alterations. PCNA is a master regulator of DNA replication and S-phase-coupled repair. PCNA post-translational modifications by ubiquitination and SUMOylation dictate how cells stabilize and re-start replication forks stalled at sites of damaged DNA.PCNAmono-ubiquitination recruits low fidelity DNA polymerases to promote error-prone replication across DNA lesions. Here, we identify the mono-ADP-ribosyltransferase PARP10/ARTD10 as a novelPCNAbinding partner. PARP10 knockdown results in genomic instability and DNA damage hypersensitivity. Importantly, we show that PARP10 binding toPCNAis required for translesionDNAsynthesis. Our work identifies a novel PCNA-linked mechanism for genome protection, centered on post-translational modification by mono-ADP-ribosylation.
Original language | English (US) |
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Pages (from-to) | 13627-13637 |
Number of pages | 11 |
Journal | Journal of Biological Chemistry |
Volume | 289 |
Issue number | 19 |
DOIs | |
State | Published - 2014 |
All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology
- Cell Biology