de Boer P A, Crossley R E, Rothfield L I
Department of Microbiology, University of Connecticut Health Center, Farmington 06030.
J Bacteriol. 1992 Jan;174(1):63-70. doi: 10.1128/jb.174.1.63-70.1992.
The proper placement of the cell division site in Escherichia coli requires the site-specific inactivation of potential division sites at the cell poles in a process that requires the coordinate action of the MinC, MinD, and MinE proteins. In the absence of MinE, the coordinate expression of MinC and MinD leads to a general inhibition of cell division. MinE gives topological specificity to the division inhibition process, so that the septation block is restricted to the cell poles. At normal levels of expression, both MinC and MinD are required for the division block. We show here that, when expressed at high levels, MinC acts as a division inhibitor even in the absence of MinD. The division inhibition that results from MinC overexpression in the absence of MinD is insensitive to the MinE topological specificity factor. The results suggest that MinC is the proximate cause of the septation block and that MinD plays two roles in the MinCDE system--it activates the MinC-dependent division inhibition mechanism and is also required for the sensitivity of the division inhibition system to the MinE topological specificity factor.
在大肠杆菌中,细胞分裂位点的正确定位需要在一个过程中对细胞两极潜在的分裂位点进行位点特异性失活,该过程需要MinC、MinD和MinE蛋白的协同作用。在没有MinE的情况下,MinC和MinD的协同表达会导致细胞分裂的普遍抑制。MinE赋予了分裂抑制过程拓扑特异性,从而使隔膜形成受阻仅限于细胞两极。在正常表达水平下,MinC和MinD对于分裂阻断都是必需的。我们在此表明,当高水平表达时,即使在没有MinD的情况下,MinC也可作为分裂抑制剂。在没有MinD时MinC过表达所导致的分裂抑制对MinE拓扑特异性因子不敏感。结果表明,MinC是隔膜形成受阻的直接原因,并且MinD在MinCDE系统中发挥两个作用——它激活依赖MinC的分裂抑制机制,并且对于分裂抑制系统对MinE拓扑特异性因子的敏感性也是必需的。