Sato T, Yura T
J Bacteriol. 1981 Jan;145(1):88-96. doi: 10.1128/jb.145.1.88-96.1981.
An ompB strain of Escherichia coli K-12 lacking major outer membrane proteins OmpC and OmpF was used to isolate a pair of mutants that have restored the ability to synthesize either OmpC or OmpF protein. These mutants were found to produce the respective proteins constitutively under the several conditions where the synthesis in the wild-type strain was markedly repressed; namely, in the absence of the ompB gene function, under restrictive medium conditions, or upon lysogenization with phage PA-2. The mutations ompCp1 and ompFp9 responsible for such synthesis were shown to be located in the close vicinity of the corresponding structural genes, ompC and ompF. Moreover, the mutations affect the expression of these genes in a cis-dominant fashion. Taken together with other evidence, it was suggested that ompCp1 and ompFp9 represent regulatory site mutations occurring at the promoter regions of ompC and ompF respectively. Relevance of these findings to the genetic control of outer membrane protein synthesis is discussed.
利用缺乏主要外膜蛋白OmpC和OmpF的大肠杆菌K-12的ompB菌株分离出一对突变体,它们恢复了合成OmpC或OmpF蛋白的能力。发现在野生型菌株中合成受到明显抑制的几种条件下,这些突变体组成型地产生各自的蛋白质;即在没有ompB基因功能的情况下、在限制性培养基条件下或在用噬菌体PA-2溶源化后。负责这种合成的突变体ompCp1和ompFp9被证明位于相应结构基因ompC和ompF的紧邻区域。此外,这些突变以顺式显性方式影响这些基因的表达。结合其他证据表明,ompCp1和ompFp9分别代表发生在ompC和ompF启动子区域的调控位点突变。讨论了这些发现与外膜蛋白合成的遗传控制的相关性。