| First Author | Logette E | Year | 2011 |
| Journal | Cell Death Differ | Volume | 18 |
| Issue | 6 | Pages | 1036-45 |
| PubMed ID | 21415862 | Mgi Jnum | J:186955 |
| Mgi Id | MGI:5433818 | Doi | 10.1038/cdd.2011.19 |
| Citation | Logette E, et al. (2011) PIDD orchestrates translesion DNA synthesis in response to UV irradiation. Cell Death Differ 18(6):1036-45 |
| abstractText | PIDD has been implicated in survival and apoptotic pathways in response to DNA damage, and a role for PIDD was recently identified in non-homologous end-joining (NHEJ) repair induced by gamma-irradiation. Here, we present an interaction of PIDD with PCNA, first identified in a proteomics screen. PCNA has essential functions in DNA replication and repair following UV irradiation. Translesion synthesis (TLS) is a process that prevents UV irradiation-induced replication blockage and is characterized by PCNA monoubiquitination and interaction with the TLS polymerase eta (poleta). Both of these processes are inhibited by p21. We report that PIDD modulates p21-PCNA dissociation, and promotes PCNA monoubiquitination and interaction with poleta in response to UV irradiation. Furthermore, PIDD deficiency leads to a defect in TLS that is associated, both in vitro and in vivo, with cellular sensitization to UV-induced apoptosis. Thus, PIDD performs key functions upon UV irradiation, including TLS, NHEJ, NF-kappaB activation and cell death. |
