Filpula D, Fuchs J A
J Bacteriol. 1977 Apr;130(1):107-13. doi: 10.1128/jb.130.1.107-113.1977.
Inhibition of deoxyribonucleic acid (DNA) synthesis in Escherichia coli by chemical inhibitors or by shifting cultures of temperature-sensitive elongation (dnaE and dnaB) or initiation (dnaA) mutants to nonpermissive conditions led to greatly increased synthesis of the enzyme ribonucleoside diphosphate reductase, which catalyzes the first reaction unique to the pathway leading to DNA replication. In contrast to the Gudas and Pardee proposed model for control of the synthesis of DNA repair enzymes, in which both DNA inhibition and DNA degradation are involved, DNA synthesis inhibition in recA, recB, recC, or lex strains results in increased synthesis of ribonucleotide reductase, which suggests that DNA degradation is not required. We propose that inhibition of DNA synthesis causes a cell to accumulate an unknown compound that stimulates the initiation of a new round of DNA replication, and that this same signal is used to induce ribonucleotide reductase synthesis.
化学抑制剂或通过将温度敏感型延伸(dnaE和dnaB)或起始(dnaA)突变体的培养物转移到非允许条件下抑制大肠杆菌中的脱氧核糖核酸(DNA)合成,导致催化DNA复制途径中第一个独特反应的核糖核苷二磷酸还原酶的合成大幅增加。与古达斯和帕迪提出的控制DNA修复酶合成的模型不同,该模型涉及DNA抑制和DNA降解,在recA、recB、recC或lex菌株中DNA合成抑制会导致核糖核苷酸还原酶合成增加,这表明不需要DNA降解。我们提出,DNA合成抑制会使细胞积累一种未知化合物,该化合物刺激新一轮DNA复制的起始,并且这个相同的信号用于诱导核糖核苷酸还原酶的合成。