Polar localization of the MinD protein of Bacillus subtilis and its role in selection of the mid-cell division site
Polar localization of the MinD protein of Bacillus subtilis and its role in selection of the mid-cell division site
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DOI：
10.1101/gad.12.21.3419
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发表时间：
1998-11-01
影响因子：
10.5
通讯作者：
Errington, J
中科院分区：
文献类型：
--
作者：
Marston, AL;Thomaides, HB;Errington, J
杆状细菌的细胞分裂是由中间细胞上形成一环的微管蛋白FtsZ启动的。分裂位点的选择是由保守的分裂抑制因子MinCD控制的，它可以防止细胞两极的异常分裂。枯草杆菌DivIVA蛋白控制着MinCD作用的拓扑特异性。在这里，我们表明DivIVA是针对它们组装后期的分裂位点，在一些需要FtsZ和其他分裂蛋白的MinCD敏感步骤已经通过之后。然后，DivIVA将大脑招募到分裂地点，防止新形成的细胞极点附近发生另一次分裂。将思想隔离到极点，也释放了下一个分裂的中间细胞位置。值得注意的是，DivIVA的这种作用机制与大肠杆菌的等效蛋白质矿完全不同，尽管这两个系统都通过相同的分裂抑制剂MinCD进行操作。
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.