Bi E, Lutkenhaus J
Department of Microbiology, Molecular Genetics, and Immunology, University of Kansas Medical Center, Kansas City 66103.
J Bacteriol. 1990 Oct;172(10):5610-6. doi: 10.1128/jb.172.10.5610-5616.1990.
In Escherichia coli, distinct but similar minicell phenotypes resulting from mutation at the minB locus and increased expression of ftsZ suggested a possible interaction between these genes. A four- to fivefold increase in FtsZ resulting from increased gene dosage was found to suppress the lethality of minCD expressed from the lac promoter. Since increased MinCD did not affect the level of FtsZ, this suggested that MinCD may antagonize FtsZ to inhibit its cell division activity. This possibility was supported by the finding that alleles of ftsZ isolated as resistant to the cell division inhibitor SulA were also resistant to MinCD. Among the ftsZ(Rsa) alleles, two appeared to be completely resistant to MinCD as demonstrated by the lack of an effect of MinCD on cell length and a minicell phenotype observed in the absence of a significant increase in FtsZ. It was shown that SulA inhibits cell division independently of MinCD.
在大肠杆菌中,由minB位点突变和ftsZ表达增加所导致的不同但相似的小细胞表型表明这些基因之间可能存在相互作用。发现基因剂量增加导致FtsZ增加四到五倍,可抑制从lac启动子表达的minCD的致死性。由于MinCD增加并不影响FtsZ的水平,这表明MinCD可能拮抗FtsZ以抑制其细胞分裂活性。ftsZ等位基因对细胞分裂抑制剂SulA具有抗性,同时也对MinCD具有抗性,这一发现支持了上述可能性。在ftsZ(Rsa)等位基因中,有两个似乎对MinCD完全抗性,这表现为MinCD对细胞长度没有影响,并且在FtsZ没有显著增加的情况下观察到小细胞表型。研究表明,SulA独立于MinCD抑制细胞分裂。