de Boer P A, Crossley R E, Rothfield L I
Department of Microbiology, University of Connecticut Health Center, Farmington 06032.
Proc Natl Acad Sci U S A. 1990 Feb;87(3):1129-33. doi: 10.1073/pnas.87.3.1129.
In Escherichia coli, selection of the proper division site at midcell requires the specific inhibition of septation at two other potential division sites, located at each of the cell poles. This site-specific inhibition of septation is mediated by the gene products of the minicell locus (the minB operon) that includes three genes, minC, minD, and minE. In this paper we show that one of the components of this division-inhibition system, the minC gene product, is also an essential component of another division-inhibition system, which is induced by derepression of the dicB gene and leads to inhibition of septation at all potential division sites. The two minC-dependent division-inhibition systems could be functionally distinguished by their different responses to the minE gene product. The results suggest a model in which a common mechanism, mediated by MinC, is responsible for the division block in a class of division-inhibition systems that can be independently activated by different proteins that determine the specific properties of these systems.
在大肠杆菌中，在细胞中部选择合适的分裂位点需要特异性抑制位于细胞两极的另外两个潜在分裂位点处的隔膜形成。这种位点特异性的隔膜形成抑制是由微细胞位点（minB操纵子）的基因产物介导的，该位点包括三个基因，即minC、minD和minE。在本文中，我们表明这种分裂抑制系统的一个组分，即minC基因产物，也是另一种分裂抑制系统的必需组分，该系统由dicB基因的去阻遏诱导，并导致所有潜在分裂位点处的隔膜形成受到抑制。这两种依赖minC的分裂抑制系统在功能上可通过它们对minE基因产物的不同反应来区分。结果提示了一个模型，其中由MinC介导的共同机制负责一类分裂抑制系统中的分裂阻滞，这些系统可由决定这些系统特异性的不同蛋白质独立激活。
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