PIDD orchestrates translesion DNA synthesis in response to UV irradiation

被引：20

作者：

Logette, E. ^{[1
]}

Schuepbach-Mallepell, S. ^{[2
]}

Eckert, M. J. ^{[1
]}

Leo, X. H. ^{[1
]}

Jaccard, B. ^{[1
]}

Manzl, C. ^{[3
]}

Tardivel, A. ^{[1
]}

Villunger, A. ^{[3
]}

Quadroni, M. ^{[4
]}

Gaide, O. ^{[3
]}

Tschopp, J. ^{[1
]}

机构：

[1] Univ Lausanne, Dept Biochem, CH-1066 Epalinges, Switzerland

[2] Geneva Med Ctr, Dept Dermatol Immunol, Geneva, Switzerland

[3] Innsbruck Med Univ, Div Dev Immunl, Bioctr, Innsbruck, Austria

[4] Univ Lausanne, Prot Anal Facil, Ctr Integrat Genom, CH-1066 Epalinges, Switzerland

来源：

CELL DEATH AND DIFFERENTIATION | 2011年 / 18卷 / 06期

关键词：

PCNA; PIDD; TLS; UV; NUCLEOTIDE EXCISION-REPAIR; NUCLEAR ANTIGEN PCNA; REPLICATION-FACTOR-C; RNA-POLYMERASE-II; COMPLEX-FORMATION; MUTATION LOAD; CLAMP LOADER; P21; DAMAGE; ETA;

D O I：

10.1038/cdd.2011.19

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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 (pol eta). Both of these processes are inhibited by p21. We report that PIDD modulates p21-PCNA dissociation, and promotes PCNA monoubiquitination and interaction with pol eta 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-kappa B activation and cell death.

引用

页码：1036 / +

页数：18

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