Bi E, Lutkenhaus J
Department of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City 66103.
J Bacteriol. 1992 Aug;174(16):5414-23. doi: 10.1128/jb.174.16.5414-5423.1992.
The ftsZ gene encodes an essential cell division protein that specifically localizes to the septum of dividing cells. In this study we characterized the effects of the ftsZ2(Rsa) mutation on cell physiology. We found that this mutation caused an altered cell morphology that included minicell formation and an increased average cell length. In addition, this mutation caused a temperature-dependent effect on cell lysis. During this investigation we fortuitously isolated a novel temperature-sensitive ftsZ mutation that consisted of a 6-codon insertion near the 5' end of the gene. This mutation, designated ftsZ26(Ts), caused an altered polar morphology at the permissive temperature and blocked cell division at the nonpermissive temperature. The altered polar morphology resulted from cell division and correlated with an altered geometry of the FtsZ ring. An intragenic cold-sensitive suppressor of ftsZ26(Ts) that caused cell lysis at the nonpermissive temperature was isolated. These results support the hypothesis that the FtsZ ring determines the division site and interacts with the septal biosynthetic machinery.
ftsZ基因编码一种必需的细胞分裂蛋白,该蛋白特异性定位于正在分裂细胞的隔膜处。在本研究中,我们表征了ftsZ2(Rsa)突变对细胞生理学的影响。我们发现这种突变导致细胞形态改变,包括微细胞形成和平均细胞长度增加。此外,这种突变对细胞裂解产生温度依赖性影响。在这项研究过程中,我们偶然分离出一种新的温度敏感型ftsZ突变,该突变由基因5'端附近的6个密码子插入组成。这种突变命名为ftsZ26(Ts),在允许温度下导致极性形态改变,在非允许温度下阻断细胞分裂。极性形态改变是由细胞分裂引起的,并与FtsZ环的几何形状改变相关。分离出ftsZ26(Ts)的基因内冷敏感抑制子,该抑制子在非允许温度下导致细胞裂解。这些结果支持以下假设:FtsZ环决定分裂位点并与隔膜生物合成机制相互作用。