Raymond-Denise A, Guillen N
Unité de Pathogénie Microbienne Moléculaire, Institut National de la Santé et de la Recherche Médicale U199, Institut Pasteur, Paris, France.
J Bacteriol. 1992 May;174(10):3171-6. doi: 10.1128/jb.174.10.3171-3176.1992.
The Bacillus subtilis dinR gene product is homologous to the LexA protein of Escherichia coli and regulates the expression of dinR and dinC. Using transcriptional fusions in the dinR and the recA genes, we have investigated the epistatic relationship between these two genes during the SOS response induced either by DNA damage or by competence. The results show that after DNA damage, induction of the expression of both recA and dinR is dependent on the activity of the DinR and RecA proteins. A RecA-dependent activity on DinR is proposed as the initial event in the induction of the SOS network. In contrast, the competence-related induction of dinR and recA appears to involve two distinct mechanisms. While one mechanism corresponds to the classical regulation of the SOS response, the other appears to involve an activating factor. Moreover, this factor is active in cells in which competence is prevented by a mutation in the regulatory gene comA.
枯草芽孢杆菌dinR基因产物与大肠杆菌的LexA蛋白同源,并调控dinR和dinC的表达。利用dinR基因和recA基因中的转录融合,我们研究了在DNA损伤或感受态诱导的SOS反应期间这两个基因之间的上位关系。结果表明,DNA损伤后,recA和dinR表达的诱导均依赖于DinR和RecA蛋白的活性。一种依赖RecA的对DinR的活性被认为是SOS网络诱导中的初始事件。相比之下,dinR和recA的感受态相关诱导似乎涉及两种不同的机制。一种机制对应于SOS反应的经典调控,另一种似乎涉及一个激活因子。此外,该因子在调控基因comA中的突变阻止感受态的细胞中具有活性。