沙门氏菌毒力的转录调控：PhoQ周质结构域突变导致向PhoP的净磷酸转移增加。
Transcriptional regulation of Salmonella virulence: a PhoQ periplasmic domain mutation results in increased net phosphotransfer to PhoP.
作者信息
Gunn J S, Hohmann E L, Miller S I
机构信息
Department of Medicine, University of Washington, Seattle 98195, USA.
出版信息
J Bacteriol. 1996 Nov;178(21):6369-73. doi: 10.1128/jb.178.21.6369-6373.1996.
Abstract
A mutation in the phoP/phoQ locus (pho-24) that results in unregulated expression of PhoP-activated genes (phenotype PhoP constitutive [PhoP(c)]) was mapped to phoQ. Change of a Thr to Ile at position 48 of PhoQ was responsible for the PhoP(c) phenotype (attenuation of mouse virulence, defects in epithelial cell invasion, and macrophage spacious phagosome formation). PhoP phosphorylation by membrane extracts required PhoQ, and PhoQ Ile-48-containing membranes demonstrated increased net phosphorylation of PhoP.
摘要
phoP/phoQ基因座（pho - 24）中的一个突变导致PhoP激活基因的表达不受调控（表型为PhoP组成型[PhoP(c)]），该突变被定位到phoQ。PhoQ第48位的苏氨酸突变为异亮氨酸导致了PhoP(c)表型（小鼠毒力减弱、上皮细胞侵袭缺陷以及巨噬细胞大吞噬体形成缺陷）。膜提取物对PhoP的磷酸化作用需要PhoQ，并且含有PhoQ异亮氨酸 - 48的膜显示出PhoP的净磷酸化增加。
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