Unconventional ubiquitin recognition by the ubiquitin-binding motif within the Y family DNA polymerases iota and Rev1.
Unconventional ubiquitin recognition by the ubiquitin-binding motif within the Y family DNA polymerases iota and Rev1.
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DOI：
10.1016/j.molcel.2009.12.038
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发表时间：
2010-02-12
期刊：
影响因子：
16
通讯作者：
Zhou P
中科院分区：
文献类型：
--
作者：
Bomar MG;D'Souza S;Bienko M;Dikic I;Walker GC;Zhou P
翻译合成是DNA损伤后促进复制的重要细胞存活策略。Y家族聚合酶（pol）1和Rev 1在停滞复制机制中的积累由聚合酶的泛素结合基序（UBM）介导，并通过PCNA单泛素化增强。我们报道了人聚合酶C-末端UBM及其与泛素复合物的溶液结构。与其他泛素结合结构域不同，UBM结合到以L 8为中心的泛素的疏水表面。因此，泛素的L 8A而不是I44 A的突变消除了UBM结合。人pol 1含有两种功能性UBM，两者都有助于复制焦点的形成。相比之下，只有酿酒酵母Rev 1的第二个UBM与泛素结合，对Rev 1依赖的细胞存活和诱变至关重要。破坏UBM-泛素相互作用的点突变也损害了体内复制灶中聚合酶1的积累和Rev 1介导的DNA损伤耐受性。
Translesion synthesis is an essential cell survival strategy to promote replication after DNA damage. The accumulation of the Y-family polymerases (pol) ι and Rev1 at the stalled replication machinery is mediated by the ubiquitin-binding motifs (UBMs) of the polymerases and enhanced by PCNA monoubiquitination. We report the solution structures of the C-terminal UBM of human pol ι and its complex with ubiquitin. Distinct from other ubiquitin-binding domains, the UBM binds to the hydrophobic surface of ubiquitin centered at L8. Accordingly, mutation of L8A, but not I44A of ubiquitin abolishes UBM binding. Human pol ι contains two functional UBMs, both of which contribute to replication foci formation. In contrast, only the second UBM of Saccharomyces cerevisiae Rev1 binds to ubiquitin and is essential for Rev1-dependent cell survival and mutagenesis. Point mutations disrupting the UBM-ubiquitin interaction also impair the accumulation of pol ι in replication foci and Rev1-mediated DNA damage tolerance in vivo.
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影响因子：
7.7
作者：
Bomar, Martha G.;Pai, Ming-Tao;Zhou, Pei
通讯作者：
Zhou, Pei
影响因子：
16
作者：
Guo, Caixia;Sonoda, Eiichiro;Friedberg, Errol C.
通讯作者：
Friedberg, Errol C.
影响因子：
3.8
作者：
Gueranger, Quentin;Stary, Anne;Weill, Jean-Claude
通讯作者：
Weill, Jean-Claude
影响因子：
8
作者：
Chang, Yong-Gang;Song, Ai-Xin;Hu, Hong-Yu
通讯作者：
Hu, Hong-Yu
Rev1与致癌物诱导的肺癌的发展有关。
DOI：
10.1158/1541-7786.mcr-08-0399
发表时间：
2009-02
期刊：
Molecular cancer research : MCR
影响因子：
--
作者：
Dumstorf CA;Mukhopadhyay S;Krishnan E;Haribabu B;McGregor WG
通讯作者：
McGregor WG