Leclerc G, Sirard C, Drapeau G R
Department of Microbiology and Immunology, Université de Montréal, Quebec, Canada.
J Bacteriol. 1989 Apr;171(4):2090-5. doi: 10.1128/jb.171.4.2090-2095.1989.
The ftsM1 mutation is believed to be in a gene implicated in the regulation of cell division in Escherichia coli because it displayed the lon mutation phenotypes. In this study, we show that this mutation is located in serU, a gene which codes for tRNA(Ser)2, and has the phenotypes of the serU allele supH. Both ftsM1 and supH suppressed the leuB6 and ilvD145 missense mutations, and both conferred temperature and UV light irradiation sensitivity to the harboring cells. Cells which carried the ftsM1 mutation or the supH suppressor had very low colony-forming abilities on salt-free L agar, and this phenotype was almost completely abolished by the presence of plasmids bearing the ftsZ+ gene. Furthermore, sensitivity of the mutant cells to UV irradiation was also markedly diminished when they carried a ftsZ+-bearing plasmid. These results suggest that supH-containing cells have reduced FtsZ activities, in accordance with their displaying the phenotypes of the lon mutant cells. The possibility that ftsM1 (supH) is functionally involved in the biosynthesis of a specific protein which affects cell division is discussed.
ftsM1突变被认为存在于一个与大肠杆菌细胞分裂调控有关的基因中，因为它表现出lon突变表型。在本研究中，我们表明该突变位于serU基因中，serU基因编码tRNA(Ser)2，且具有serU等位基因supH的表型。ftsM1和supH都抑制了leuB6和ilvD145错义突变，并且都使携带它们的细胞对温度和紫外线照射敏感。携带ftsM1突变或supH抑制子的细胞在无盐L琼脂上的集落形成能力非常低，而携带ftsZ+基因的质粒的存在几乎完全消除了这种表型。此外，当突变细胞携带含有ftsZ+的质粒时，它们对紫外线照射的敏感性也显著降低。这些结果表明，含有supH的细胞具有降低的FtsZ活性，这与它们表现出lon突变细胞的表型一致。本文还讨论了ftsM1（supH）在功能上参与影响细胞分裂的特定蛋白质生物合成的可能性。
