Marston A L, Thomaides H B, Edwards D H, Sharpe M E, Errington J
Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
Genes Dev. 1998 Nov 1;12(21):3419-30. doi: 10.1101/gad.12.21.3419.
Cell division in rod-shaped bacteria is initiated by formation of a ring of the tubulin-like protein FtsZ at mid-cell. Division site selection is controlled by a conserved division inhibitor MinCD, which prevents aberrant division at the cell poles. The Bacillus subtilis DivIVA protein controls the topological specificity of MinCD action. Here we show that DivIVA is targeted to division sites late in their assembly, after some MinCD-sensitive step requiring FtsZ and other division proteins has been passed. DivIVA then recruits MinD to the division sites preventing another division from taking place near the newly formed cell poles. Sequestration of MinD to the poles also releases the next mid-cell sites for division. Remarkably, this mechanism of DivIVA action is completely different from that of the equivalent protein MinE of Escherichia coli, even though both systems operate via the same division inhibitor MinCD.
杆状细菌中的细胞分裂是由一种微管蛋白样蛋白FtsZ在细胞中部形成环而启动的。分裂位点的选择由一种保守的分裂抑制剂MinCD控制，它可防止细胞两极出现异常分裂。枯草芽孢杆菌的DivIVA蛋白控制着MinCD作用的拓扑特异性。我们在此表明，DivIVA在分裂位点组装后期被靶向定位，此时已经经过了一些需要FtsZ和其他分裂蛋白参与的MinCD敏感步骤。然后，DivIVA将MinD招募到分裂位点，防止在新形成的细胞两极附近发生另一次分裂。将MinD隔离到两极也会释放出下一个用于分裂的细胞中部位点。值得注意的是，DivIVA的这种作用机制与大肠杆菌中同源蛋白MinE的机制完全不同，尽管这两个系统都是通过相同的分裂抑制剂MinCD起作用。
