Bacillus subtilis EzrA and FtsL synergistically regulate FtsZ ring dynamics during cell division
Bacillus subtilis EzrA and FtsL synergistically regulate FtsZ ring dynamics during cell division
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DOI：
10.1099/mic.0.28497-0
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发表时间：
2006-04-01
期刊：
影响因子：
2.8
通讯作者：
Ogasawara, N
中科院分区：
文献类型：
--
作者：
Kawai, Y;Ogasawara, N
先前的工作已经表明，枯草芽孢杆菌EzrA蛋白直接抑制FtsZ环组装，这是正常细胞分裂所需的，并且EzrA的缺失导致体内FtsZ聚合物的超稳定。在此，发现在ezrA破坏的细胞中，在SOS响应期间抑制细胞分裂的YneA的人工表达和作为类核封闭效应物的noc（yyaA）的破坏导致多个非收缩FtsZ环的积累、细胞分裂的抑制和合成致死性。过表达的必需的细胞分裂蛋白FtsL抑制ezrA中断的效果。FtsL过表达恢复了在ezrA破坏的野生型细胞中观察到的延迟的FtsZ环收缩。相反，EzrA的缺乏导致产生比野生型细胞更低量的FtsL的细胞的致死性。以前有报道称，FtsL在细胞分裂的后期被募集到分裂位点，尽管其确切作用目前尚不清楚。本研究的结果表明，FtsL和EzrA协同调节FtsZ环收缩在B。枯草杆菌。有趣的是，FtsL过表达也抑制了细胞分裂抑制由于YneA表达或Noc失活在ezrA破坏的细胞。
Previous work has shown that the Bacillus subtilis EzrA protein directly inhibits FtsZ ring assembly, which is required for normal cell division, and that loss of EzrA results in hyperstabilization of the FtsZ polymer in vivo. Here, it was found that in ezrA-disrupted cells, artificial expression of YneA, which suppresses cell division during the SOS response, and disruption of noc (yyaA), which acts as an effector of nucleoid occlusion, resulted in accumulation of multiple non-constricting FtsZ rings, inhibition of cell division, and synthetic lethality. Overexpression of the essential cell division protein FtsL suppressed the effect of ezrA disruption. FtsL overexpression recovered the delayed FtsZ ring constriction seen in ezrA-disrupted wild-type cells. Conversely, the absence of EzrA caused lethality in cells producing a lower amount of FtsL than wild-type cells. It has previously been reported that FtsL is recruited to the division site during the later stages of cell division, although its exact role is currently unknown. The results of this study suggest that FtsL and EzrA synergistically regulate the FtsZ ring constriction in B. subtilis. Interestingly, FtsL overexpression also suppressed the cell division inhibition due to YneA expression or Noc inactivation in ezrA-disrupted cells.