Waters Lauren S, Minesinger Brenda K, Wiltrout Mary Ellen, D'Souza Sanjay, Woodruff Rachel V, Walker Graham C
Department of Biology, Massachusetts Institute of Technology, Building 68, Room 653, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
Microbiol Mol Biol Rev. 2009 Mar;73(1):134-54. doi: 10.1128/MMBR.00034-08.
DNA repair and DNA damage tolerance machineries are crucial to overcome the vast array of DNA damage that a cell encounters during its lifetime. In this review, we summarize the current state of knowledge about the eukaryotic DNA damage tolerance pathway translesion synthesis (TLS), a process in which specialized DNA polymerases replicate across from DNA lesions. TLS aids in resistance to DNA damage, presumably by restarting stalled replication forks or filling in gaps that remain in the genome due to the presence of DNA lesions. One consequence of this process is the potential risk of introducing mutations. Given the role of these translesion polymerases in mutagenesis, we discuss the significant regulatory mechanisms that control the five known eukaryotic translesion polymerases: Rev1, Pol zeta, Pol kappa, Pol eta, and Pol iota.
DNA修复和DNA损伤耐受机制对于克服细胞在其生命周期中遇到的大量DNA损伤至关重要。在本综述中，我们总结了关于真核生物DNA损伤耐受途径跨损伤合成（TLS）的当前知识状态，这是一个特殊的DNA聚合酶跨越DNA损伤进行复制的过程。TLS有助于抵抗DNA损伤，推测是通过重新启动停滞的复制叉或填补由于DNA损伤的存在而留在基因组中的缺口。这个过程的一个后果是引入突变的潜在风险。鉴于这些跨损伤聚合酶在诱变中的作用，我们讨论了控制五种已知真核生物跨损伤聚合酶的重要调控机制：Rev1、Pol ζ、Pol κ、Pol η和Pol ι。
