Siegele D A, Imlay K R, Imlay J A
Department of Biology, Texas A&M University, College Station 77843-3258, USA.
J Bacteriol. 1996 Nov;178(21):6091-6. doi: 10.1128/jb.178.21.6091-6096.1996.
The surB gene was identified as a gene product required for Escherichia coli cells to exit stationary phase at 37 degrees C under aerobic conditions. surB was shown to be the same as cydC, whose product is required for the proper assembly and activity of cytochrome d oxidase. Cytochrome d oxidase, encoded by the cydAB operon, is one of two alternate terminal cytochrome oxidases that function during aerobic electron transport in E. coli. Mutations inactivating the cydAB operon also cause a temperature-sensitive defect in exiting stationary phase, but the phenotype is not as severe as it is for surB mutants. In this study, we examined the phenotypes of surB1 delta(cydAB) double mutants and the ability of overexpression of cytochrome o oxidase to suppress the temperature-sensitive stationary-phase-exit defect of surB1 and delta(cydAB) mutants and analyzed spontaneous suppressors of surB1. Our results indicate that the severe temperature-sensitive defect in exiting stationary phase of surB1 mutants is due both to the absence of terminal cytochrome oxidase activity and to the presence of a defective cytochrome d oxidase. Membrane vesicles prepared from wild-type, surB1, and delta(cydAB) strains produced superoxide radicals at the same rate in vitro. Therefore, the aerobic growth defects of the surB1 and delta(cydAB) strains are not due to enhanced superoxide production resulting from the block in aerobic electron transport.
surB基因被鉴定为大肠杆菌细胞在有氧条件下于37℃退出稳定期所必需的基因产物。已证明surB与cydC相同,其产物是细胞色素d氧化酶正确组装和活性所必需的。由cydAB操纵子编码的细胞色素d氧化酶是大肠杆菌有氧电子传递过程中起作用的两种交替末端细胞色素氧化酶之一。使cydAB操纵子失活的突变也会导致退出稳定期时出现温度敏感缺陷,但该表型不如surB突变体严重。在本研究中,我们检测了surB1Δ(cydAB)双突变体的表型以及细胞色素o氧化酶过表达抑制surB1和Δ(cydAB)突变体温度敏感型稳定期退出缺陷的能力,并分析了surB1的自发抑制子。我们的结果表明,surB1突变体退出稳定期时严重的温度敏感缺陷既归因于末端细胞色素氧化酶活性的缺失,也归因于有缺陷的细胞色素d氧化酶的存在。从野生型、surB1和Δ(cydAB)菌株制备的膜囊泡在体外以相同速率产生超氧自由基。因此,surB1和Δ(cydAB)菌株的有氧生长缺陷并非由于有氧电子传递受阻导致超氧产生增加。