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Eukaryotic polymerases ι and ζ act sequentially to bypass DNA lesions

机译：真核聚合酶η和ζ依次起作用以绕过DNA损伤

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摘要

DNA lesions can often block DNA replication, so cells possess specialized low-fidelity, and often error-prone, DNA polymerases that can bypass such lesions and promote replication of damaged DNA. The Saccharomyces cerevisiae RAD30 and human hRAD30A encode Polη, which bypasses a cis-syn thymine-thymine dimer efficiently and accurately. Here we show that a related human gene, hRAD30B, encodes the DNA polymerase Polι, which misincorporates deoxynucleotides at a high rate. To bypass damage, Polι specifically incorporates deoxynucleotides opposite highly distorting or non-instructional DNA lesions. This action is combined with that of DNA polymerase Polζ, which is essential for damage-induced mutagenesis, to complete the lesion bypass. Polζ is very inefficient in inserting deoxynucleotides opposite DNA lesions, but readily extends from such deoxynu-cleotides once they have been inserted. Thus, in a new model for mutagenic bypass of DNA lesions in eukaryotes, the two DNA polymerases act sequentially: Polι incorporates deoxynucleotides opposite DNA lesions, and Polζ functions as a mispair extender.
机译：DNA损伤通常会阻止DNA复制，因此细胞具有特殊的低保真且经常容易出错的DNA聚合酶，可以绕过此类损伤并促进受损DNA的复制。酿酒酵母RAD30和人类hRAD30A编码Polη，其有效且准确地绕过顺式-胸腺嘧啶-胸腺嘧啶二聚体。在这里，我们显示了相关的人类基因hRAD30B编码DNA聚合酶Pol1，后者以很高的比率错误地掺入了脱氧核苷酸。为了绕过损害，Polι特异地掺入了与高度失真或非指导性DNA损伤相对的脱氧核苷酸。该作用与DNA聚合酶Polζ的作用结合在一起，这对损伤诱导的诱变至关重要，以完成病变旁路。 Polζ在插入与DNA损伤相对的脱氧核苷酸方面效率非常低，但是一旦被插入，就很容易从这种脱氧核苷酸中延伸出来。因此，在用于真核生物中DNA损伤的诱变绕过的新模型中，两种DNA聚合酶顺序地起作用：Pol 1掺入了与DNA损伤相对的脱氧核苷酸，而Polζ作为错配对的延伸物。

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