Gervais F G, Phoenix P, Drapeau G R
Department of Microbiology, Université de Montréal, Québec, Canada.
J Bacteriol. 1992 Jun;174(12):3964-71. doi: 10.1128/jb.174.12.3964-3971.1992.
Wild-type genes which, when overexpressed, are capable of restoring the growth deficiency of the division mutant ftsZ84 of Escherichia coli on L medium containing no added NaCl have been isolated. One of these genes is rcsB, a positive regulator of colanic acid biosynthesis. A direct relationship between rcsB expression and FtsZ activity was observed, suggesting that RcsB specifically increases transcription of ftsZ, thus accounting for the restoration of colony formation by ftsZ84 mutant cells. Analysis of the 5' upstream sequence of rcsB revealed, in addition to the sigma 54 promoter sequence previously reported, a presumptive sigma 70 promoter and LexA-binding site plus an upstream sequence that is found to be essential for the expression of rcsB on a plasmid. The absence of the sigma 54 factor does not have a negative effect on the transcription of rcsB. The RcsB protein is an activator of its own synthesis, particularly in the presence of NaCl. Evidence which suggests that RcsB can be phosphorylated by a presumably modified EnvZ or PhoM sensor protein leading to a suppression of the growth deficiency of ftsZ84 mutant cells and to an increase in colanic acid production was obtained. We also demonstrated that the level of colanic acid is reduced when the cells carry a multicopy rcsC plasmid, suggesting that the RcsC sensor has phosphatase activity.
已分离出野生型基因，当这些基因过表达时，能够恢复大肠杆菌分裂突变体ftsZ84在不添加氯化钠的L培养基上的生长缺陷。其中一个基因是rcsB，它是荚膜酸生物合成的正调控因子。观察到rcsB表达与FtsZ活性之间存在直接关系，这表明RcsB特异性地增加ftsZ的转录，从而解释了ftsZ84突变细胞菌落形成的恢复。对rcsB的5'上游序列分析表明，除了先前报道的σ54启动子序列外，还有一个推测的σ70启动子和LexA结合位点，以及一个发现对质粒上rcsB表达至关重要的上游序列。σ54因子的缺失对rcsB的转录没有负面影响。RcsB蛋白是其自身合成的激活剂，尤其是在有氯化钠存在的情况下。有证据表明，RcsB可能被一种可能经过修饰的EnvZ或PhoM传感蛋白磷酸化，从而导致ftsZ84突变细胞生长缺陷的抑制和荚膜酸产量的增加。我们还证明，当细胞携带多拷贝rcsC质粒时，荚膜酸水平会降低，这表明RcsC传感蛋白具有磷酸酶活性。
