DNA damage-induced mutation: tolerance via translesion synthesis

被引:57
作者
Kunz, BA [1 ]
Straffon, AFL [1 ]
Vonarx, EJ [1 ]
机构
[1] Deakin Univ, Sch Biol & Chem Sci, Geelong, Vic 3217, Australia
基金
加拿大自然科学与工程研究理事会; 澳大利亚研究理事会;
关键词
DNA damage; translesion synthesis; DNA polymerase eta; DNA polymerase xi; yeast; mammalian cells;
D O I
10.1016/S0027-5107(00)00048-8
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Translesion synthesis (TLS) appears to be required for most damage-induced mutagenesis in the yeast Saccharomyces cerevisiae, whether the damage arises from endogenous or exogenous sources. Thus, the production of such mutations seems to occur primarily as a consequence of the tolerance of DNA lesions rather than an error-prone repair mechanism. Tolerance via TLS in yeast involves proteins encoded by members of the RAD6 epistasis group for the repair of ultraviolet (UV) photoproducts, in particular two non-essential DNA polymerases that catalyse error-free or error-prone TLS. Homologues of these RAD6 group proteins have recently been discovered in rodent and/or human cells. Furthermore, the operation of error-free TLS in humans has been linked to a reduced risk of W-induced skin cancer, whereas mutations generated by error-prone TLS may increase the risk of cancer. In this article, we review and link the evidence for translesion synthesis in yeast and the involvement of nonreplicative DNA polymerases, to recent findings in mammalian cells. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:169 / 185
页数:17
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