Sedgwick S G, Goodwin P A
Proc Natl Acad Sci U S A. 1985 Jun;82(12):4172-6. doi: 10.1073/pnas.82.12.4172.
The incidence of recombinational DNA repair and inducible mutagenic DNA repair has been examined in Escherichia coli and 11 related species of enterobacteria. Recombinational repair was found to be a common feature of the DNA repair repertoire of at least 6 genera of enterobacteria. This conclusion is based on observations of (i) damage-induced synthesis of RecA-like proteins, (ii) nucleotide hybridization between E. coli recA sequences and some chromosomal DNAs, and (iii) recA-negative complementation by plasmids showing SOS-inducible expression of truncated E. coli recA genes. The mechanism of DNA damage-induced gene expression is therefore sufficiently conserved to allow non-E. coli regulatory elements to govern expression of these cloned truncated E. coli recA genes. In contrast, the process of mutagenic repair, which uses umuC+ umuD+ gene products in E. coli, appeared less widespread. Little ultraviolet light-induced mutagenesis to rifampicin resistance was detected outside the genus Escherichia, and even within the genus induced mutagenesis was detected in only 3 out of 6 species. Nucleotide hybridization showed that sequences like the E. coli umuCD+ gene are not found in these poorly mutable organisms. Evolutionary questions raised by the sporadic incidence of inducible mutagenic repair are discussed.
在大肠杆菌和11种相关肠杆菌属细菌中,对重组DNA修复和诱导性诱变DNA修复的发生率进行了检测。发现重组修复是至少6个肠杆菌属细菌DNA修复机制中的一个共同特征。这一结论基于以下观察结果:(i)损伤诱导的类RecA蛋白的合成;(ii)大肠杆菌recA序列与一些染色体DNA之间的核苷酸杂交;(iii)携带截短的大肠杆菌recA基因且具有SOS诱导表达的质粒对recA阴性菌株的互补作用。因此,DNA损伤诱导的基因表达机制具有足够的保守性,使得非大肠杆菌的调控元件能够控制这些克隆的截短大肠杆菌recA基因的表达。相比之下,在大肠杆菌中利用umuC+umuD+基因产物的诱变修复过程似乎分布不那么广泛。在大肠杆菌属以外,几乎检测不到紫外线诱导的对利福平抗性的诱变,即使在大肠杆菌属内,6个物种中也只有3个检测到诱导诱变。核苷酸杂交表明,在这些诱变能力较弱的生物体中未发现类似大肠杆菌umuCD+基因的序列。文中还讨论了诱导性诱变修复的零星发生率所引发的进化问题。