Bridges B A
MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.
Mol Gen Genet. 1992 Jun;233(3):331-6. doi: 10.1007/BF00265428.
The induction of mutations by ultraviolet light and delayed photoreversal in bacteria defective for SOS mutagenesis is discussed in terms of two models: the two-step misincorporation and bypass model, and the model involving simple deamination of cytosine-containing dimers. In phage S13 the latter appears to be the predominant mechanism. In Escherichia coli there is little evidence that the simple deamination mechanism is of any significance except in ung strains lacking uracil glycosylase where uracils left after photoreversal are not removed. Deamination might, however, occur during the operation of translesion synthesis via the two-step model and if it did, subsequent photoreversal would lead to the "mutation" being extended from one to both strands by uracil glycosylase repair rather than being removed.
本文根据两种模型讨论了紫外线诱导细菌突变以及SOS诱变缺陷型细菌中的延迟光逆转现象:两步错配掺入和旁路模型,以及涉及含胞嘧啶二聚体简单脱氨基作用的模型。在噬菌体S13中,后一种模型似乎是主要机制。在大肠杆菌中,几乎没有证据表明简单脱氨基机制具有任何重要意义,除非在缺乏尿嘧啶糖基化酶的ung菌株中,光逆转后留下的尿嘧啶不会被去除。然而,脱氨基作用可能在通过两步模型进行跨损伤合成的过程中发生,如果发生这种情况,随后的光逆转将导致“突变”通过尿嘧啶糖基化酶修复从一条链扩展到两条链,而不是被去除。