Witkin E M
Basic Life Sci. 1975;5A:369-78. doi: 10.1007/978-1-4684-2895-7_49.
DNA damage triggers coordinate expression of a cluster of diverse functions in Escherichia coli, including prophage induction, filamentous growth, and "aberrant" reintiation of DNA replication at the chromosomal origin. The "SOS repair" hypothesis proposes that one of these coordinately inducible functions is an error-prone system of DNA repair ("SOS repair") which is responsible for ultraviolet mutagenesis. In dnaB strains, incubation of 42 degrees C stops DNA synthesis and induces lambda prophage and should, therefore, also induce the postulated error-prone repair activity. Thermal posttreatment of a dnaB urvA derivative of E. coli B/r is found to enhance the yield of ultraviolet-light-induced mutations as much as 50-fold, while having no such effect in the dnaB+ parent strain. The results support the SOS repair hypothesis. The possibility is discussed that the inducible repair system is a mutagenic DNA polymerase.
DNA损伤会引发大肠杆菌中一系列不同功能的协同表达，包括原噬菌体诱导、丝状生长以及染色体复制起点处DNA复制的“异常”重新起始。“SOS修复”假说提出，这些协同诱导功能之一是一种易出错的DNA修复系统（“SOS修复”），它负责紫外线诱变。在dnaB菌株中，42℃孵育会停止DNA合成并诱导λ原噬菌体，因此也应该诱导假定的易出错修复活性。发现对大肠杆菌B/r的dnaB urvA衍生物进行热后处理可使紫外线诱导的突变率提高多达50倍，而在dnaB+亲本菌株中则没有这种效果。这些结果支持了SOS修复假说。文中还讨论了诱导性修复系统是一种诱变DNA聚合酶的可能性。
