Mileykovskaya E, Dowhan W
Department of Biochemistry and Molecular Biology, University of Texas Houston-Medical School, 77225, USA.
J Bacteriol. 1997 Feb;179(4):1029-34. doi: 10.1128/jb.179.4.1029-1034.1997.
The CpxA-CpxR two-component signal transduction pathway of Escherichia coli was studied in a mutant (pss-93) lacking phosphatidylethanolamine (PE). Several properties of this mutant are comparable to phenotypes of cpxA point mutants, indicating that this two-component pathway is activated in PE-deficient cells. In contrast to point mutants, cpx operon null mutants have a wild-type phenotype. By use of this information, a cpx operon null allele was introduced into a pss-93 mutant. Certain altered properties of PE-deficient mutants, which were consistent with activation of the Cpx pathway, returned to the wild-type phenotype, namely, active accumulation of proline and thiomethyl-beta-D-galactopyranoside was partially restored to wild-type levels, increased resistance to amikacin returned to wild-type sensitivity, and high levels of degP expression returned to repressed wild-type levels. Elevated levels of acetyl phosphate and nlpE gene product can result in activation of the Cpx pathway. However, inactivation of the nlpE gene or mutations eliminating the ability to make acetyl phosphate did not alter the high level of degP expression in pss-93 mutants. We propose that the lack of PE results in an alteration in cell envelope structure or physical properties, leading to direct activation of the Cpx pathway.
在缺乏磷脂酰乙醇胺（PE）的突变体（pss - 93）中研究了大肠杆菌的CpxA - CpxR双组分信号转导途径。该突变体的几个特性与cpxA点突变体的表型相当，表明该双组分途径在PE缺陷型细胞中被激活。与点突变体不同，cpx操纵子缺失突变体具有野生型表型。利用这一信息，将一个cpx操纵子缺失等位基因导入pss - 93突变体中。PE缺陷型突变体的某些改变的特性，这些特性与Cpx途径的激活一致，恢复到了野生型表型，即脯氨酸和硫代甲基 - β - D - 吡喃半乳糖苷的活性积累部分恢复到野生型水平，对阿米卡星的抗性增加恢复到野生型敏感性，并且degP的高表达水平恢复到野生型的抑制水平。乙酰磷酸和nlpE基因产物水平的升高可导致Cpx途径的激活。然而，nlpE基因的失活或消除产生乙酰磷酸能力的突变并没有改变pss - 93突变体中degP的高表达水平。我们提出，PE的缺乏导致细胞包膜结构或物理性质的改变，从而导致Cpx途径的直接激活。
