Evidence for functional overlap among multiple bacterial cell division proteins: compensating for the loss of FtsK
Evidence for functional overlap among multiple bacterial cell division proteins: compensating for the loss of FtsK
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DOI：
10.1111/j.1365-2958.2005.04858.x
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发表时间：
2005-10-01
影响因子：
3.6
通讯作者：
Margolin, W
中科院分区：
文献类型：
--
作者：
Geissler, B;Margolin, W
在大肠杆菌中，至少有12种蛋白质共定位于细胞中点，组装成形成分裂隔膜的膜相关蛋白机器。这些蛋白质中的许多，包括FtsK，是生存所必需的，但它们在细胞分裂中的功能是未知的。在这里，我们表明，FtsK在细胞分裂中的基本功能可以部分绕过。含有ftsA R286 W突变或携带ftsQAZ基因的质粒的细胞有效地抑制了ftsK 44（ts）等位基因。此外，ftsA R286 W或多拷贝ftsQAZ可以在很大程度上绕过对必需的细胞分裂基因zipA的要求，允许ftsK完全缺失的细胞存活和分裂，尽管这些ftsK缺失细胞中的许多形成多分隔链。绿色荧光蛋白（GFP）融合到FtsI和FtsN，这通常依赖于FtsK定位到分裂位点，定位到分裂位点在FtsK的情况下，表明FtsK是不直接参与其招聘。细胞表达额外的ftsQ，并在较小程度上ftsB和ftsN，能够生存和分裂的ftsK的情况下，虽然细胞链往往形成。令人惊讶的是，FtsQ的胞质和跨膜结构域，虽然不足以补充ftsQ无效突变体，但在不存在ftsK的情况下赋予活力和隔膜形成。这些发现表明，FtsK的N-末端结构域通常参与分裂蛋白机器的稳定性，并与FtsQ，FtsB，FtsA，ZipA和FtsN共享功能重叠。
In Escherichia coli, at least 12 proteins colocalize to the cell midpoint, assembling into a membrane-associated protein machine that forms the division septum. Many of these proteins, including FtsK, are essential for viability but their functions in cell division are unknown. Here we show that the essential function of FtsK in cell division can be partially bypassed. Cells containing either the ftsA R286W mutation or a plasmid carrying the ftsQAZ genes suppressed a ftsK44(ts) allele efficiently. Moreover, ftsA R286W or multicopy ftsQAZ, which can largely bypass the requirement for the essential cell division gene zipA, allowed cells with a complete deletion of ftsK to survive and divide, although many of these ftsK null cells formed multiseptate chains. Green fluorescent protein (GFP) fusions to FtsI and FtsN, which normally depend on FtsK to localize to division sites, localized to division sites in the absence of FtsK, indicating that FtsK is not directly involved in their recruitment. Cells expressing additional ftsQ, and to a lesser extent ftsB and ftsN, were able to survive and divide in the absence of ftsK, although cell chains were often formed. Surprisingly, the cytoplasmic and transmembrane domains of FtsQ, while not sufficient to complement an ftsQ null mutant, conferred viability and septum formation in the absence of ftsK. These findings suggest that the N-terminal domain of FtsK is normally involved in stability of the division protein machine and shares functional overlap with FtsQ, FtsB, FtsA, ZipA and FtsN.