Huang C, Stewart R C
Department of Microbiology and Immunology, McGill University, Montreal, Québec, Canada.
Biochim Biophys Acta. 1993 Oct 6;1202(2):297-304. doi: 10.1016/0167-4838(93)90019-n.
CheZ is a component of the chemotaxis signal-transduction pathway in Escherichia coli and Salmonella typhimurium. It is responsible for accelerating dephosphorylation of CheY and thereby antagonizing the tumble-promoting activity of CheY. In the absence of functional CheZ, cells are non-chemotactic and tumble constantly. We characterized the effects of two mutations in CheZ, R54C and V166G, that are unusual in that they cause cells to have a smooth swimming bias. These mutations were isolated as second-site suppressors of mutations in the switch complex responsible for regulating the direction of flagellar rotation (Yamaguchi, S., Aizawa, S.-I., Kihara, M. Isomura, M., Jones, C.J. and Macnab, R.M. (1986) J. Bacteriol. 168, 1172-1179). When produced at low levels in a delta cheZ host strain, CheZ R54C and CheZ V166G supported chemotaxis. However, when moderately overproduced they markedly inhibited chemotactic ability. In vitro studies revealed that these mutations enhanced the ability of CheZ to accelerate dephosphorylation of CheY. These results are discussed in relation to the possible roles and interactions of CheZ in the chemotaxis system.
CheZ是大肠杆菌和鼠伤寒沙门氏菌趋化信号转导途径的一个组成部分。它负责加速CheY的去磷酸化，从而对抗CheY促进翻滚的活性。在缺乏功能性CheZ的情况下，细胞无趋化性且持续翻滚。我们对CheZ中的两个突变R54C和V166G的影响进行了表征，这两个突变不同寻常之处在于它们使细胞具有平滑游动偏向性。这些突变是作为负责调节鞭毛旋转方向的开关复合体中突变的第二位点抑制子分离得到的（山口，S.，相泽，S.-I.，木原，M.，矶村，M.，琼斯，C.J.和麦克纳布，R.M.（1986年）《细菌学杂志》168，1172 - 1179）。当在ΔcheZ宿主菌株中低水平表达时，CheZ R54C和CheZ V166G支持趋化作用。然而，当适度过量表达时，它们会显著抑制趋化能力。体外研究表明，这些突变增强了CheZ加速CheY去磷酸化的能力。结合CheZ在趋化系统中可能的作用和相互作用对这些结果进行了讨论。
