Kaniga K, Tucker S, Trollinger D, Galán J E
Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook 11794-5222, USA.
J Bacteriol. 1995 Jul;177(14):3965-71. doi: 10.1128/jb.177.14.3965-3971.1995.
Entry into host cells is an essential feature in the pathogenicity of Salmonella spp. The inv locus of Salmonella typhimurium encodes several proteins which are components of a type III protein secretion system required for these organisms to gain access to host cells. We report here the identification of several proteins whose secretion into the culture supernatant of S. typhimurium is dependent on the function of the inv-encoded translocation apparatus. Nucleotide sequence analysis of the genes encoding two of these secreted proteins, SipB and SipC, indicated that they are homologous to the Shigella sp. invasins IpaB and IpaC, respectively. An additional gene was identified, sicA, which encodes a protein homologous to IpgC, a Shigella protein that serves as a molecular chaperone for the invasins IpaB and IpaC. Nonpolar mutations in sicA, sipB, and sipC rendered S. typhimurium unable to enter cultured epithelial cells, indicating that these genes are required for bacterial internalization.
进入宿主细胞是沙门氏菌致病性的一个基本特征。鼠伤寒沙门氏菌的inv基因座编码几种蛋白质，这些蛋白质是这些细菌进入宿主细胞所需的III型蛋白质分泌系统的组成部分。我们在此报告了几种蛋白质的鉴定，它们分泌到鼠伤寒沙门氏菌培养上清液中依赖于inv编码的转运装置的功能。对编码其中两种分泌蛋白SipB和SipC的基因进行核苷酸序列分析表明，它们分别与志贺氏菌属入侵蛋白IpaB和IpaC同源。还鉴定出一个额外的基因sicA，它编码一种与IpgC同源的蛋白质，IpgC是一种志贺氏菌蛋白质，作为入侵蛋白IpaB和IpaC的分子伴侣。sicA、sipB和sipC中的非极性突变使鼠伤寒沙门氏菌无法进入培养的上皮细胞，表明这些基因是细菌内化所必需的。
