Bacterial Membrane Proteomics Laboratory, Instituto de Tecnologia Química e Biológica, Universidade Nova de Lisboa, Oeiras, Portugal.
PLoS One. 2010 Aug 11;5(8):e12048. doi: 10.1371/journal.pone.0012048.
Cell division in Bacillus subtilis occurs precisely at midcell. Positional control of cell division is exerted by two mechanisms: nucleoid occlusion, through Noc, which prevents division through nucleoids, and the Min system, where the combined action of the MinC, D and J proteins prevents formation of the FtsZ ring at cell poles or recently completed division sites.
METHODOLOGY/PRINCIPAL FINDINGS: We used a genetic screen to identify mutations in ftsZ that confer resistance to the lethal overexpression of the MinC/MinD division inhibitor. The FtsZ mutants were purified and found to polymerize to a similar or lesser extent as wild type FtsZ, and all mutants displayed reduced GTP hydrolysis activity indicative of a reduced polymerization turnover. We found that even though the mutations conferred in vivo resistance to MinC/D, the purified FtsZ mutants did not display strong resistance to MinC in vitro.
CONCLUSIONS/SIGNIFICANCE: Our results show that in B. subtilis, overproduction of MinC can be countered by mutations that alter FtsZ polymerization dynamics. Even though it would be very likely that the FtsZ mutants found depend on other Z-ring stabilizing proteins such as ZapA, FtsA or SepF, we found this not to be the case. This indicates that the cell division process in B. subtilis is extremely robust.
枯草芽孢杆菌的细胞分裂精确发生在细胞中部。细胞分裂的位置控制是通过两种机制实现的：核区遮挡，通过 Noc 防止核区通过，以及 Min 系统，其中 MinC、D 和 J 蛋白的联合作用防止 FtsZ 环在细胞极或最近完成的分裂部位形成。
方法/主要发现：我们使用遗传筛选来鉴定赋予 FtsZ 突变体对 MinC/MinD 分裂抑制剂的致死过表达抗性的突变。纯化 FtsZ 突变体并发现其聚合程度与野生型 FtsZ 相似或更低，并且所有突变体都显示出降低的 GTP 水解活性，表明聚合周转率降低。我们发现，尽管这些突变赋予了体内对 MinC/D 的抗性，但纯化的 FtsZ 突变体在体外并不对 MinC 表现出很强的抗性。
结论/意义：我们的结果表明，在枯草芽孢杆菌中，过表达 MinC 可以通过改变 FtsZ 聚合动力学的突变来对抗。即使 FtsZ 突变体很可能依赖于其他 Z 环稳定蛋白，如 ZapA、FtsA 或 SepF，但事实并非如此。这表明枯草芽孢杆菌的细胞分裂过程非常稳健。
