Nagahama Hideki, Sakamoto Yutaka, Matsumoto Kouji, Hara Hiroshi
Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, Japan.
J Gen Appl Microbiol. 2006 Apr;52(2):91-8. doi: 10.2323/jgam.52.91.
In the Escherichia coli pgsA null mutant, which lacks the major acidic phospholipids, the Rcs phosphorelay signal transduction system is activated, causing thermosensitive growth. The mutant grows poorly at 37 degrees C and lyses at 42 degrees C. We showed that the poor growth at 37 degrees C was corrected by disruption of the rcsA gene, which codes for a coregulator protein that interacts with the RcsB response regulator of the phosphorelay system. However, mutant cells still lysed when incubated at 42 degrees C even in the absence of RcsA. We conclude that the activated Rcs phosphorelay in the pgsA null mutant has both RcsA-dependent and -independent growth inhibitory effects. Since the Rcs system has been shown to positively regulate the essential cell division genes ftsA and ftsZ independently of RcsA, we measured cellular levels of the FtsZ protein, but found that the growth defect of the mutant at 42 degrees C did not involve a change in the level of this protein.
在缺乏主要酸性磷脂的大肠杆菌pgsA基因敲除突变体中，Rcs磷信号转导系统被激活，导致温度敏感型生长。该突变体在37℃时生长不良，在42℃时裂解。我们发现，rcsA基因（编码一种与磷信号系统的RcsB应答调节因子相互作用的共调节蛋白）的破坏纠正了37℃时的生长不良。然而，即使在没有RcsA的情况下，突变细胞在42℃孵育时仍会裂解。我们得出结论，pgsA基因敲除突变体中激活的Rcs磷信号转导具有RcsA依赖性和非依赖性生长抑制作用。由于已证明Rcs系统可独立于RcsA正向调节必需的细胞分裂基因ftsA和ftsZ，我们测量了FtsZ蛋白的细胞水平，但发现突变体在42℃时的生长缺陷并不涉及该蛋白水平的变化。
