Adler B, Sasakawa C, Tobe T, Makino S, Komatsu K, Yoshikawa M
Department of Bacteriology, Institute of Medical Science, University of Tokyo, Japan.
Mol Microbiol. 1989 May;3(5):627-35. doi: 10.1111/j.1365-2958.1989.tb00210.x.
The expression of plasmid-encoded, invasion-related antigens lpa b, c and d of Shigella flexneri was found to be positively regulated at transcriptional level by a 33kD protein produced by the previously defined, virulence-associated Region 1 on the SalI fragment B of the 230 kb invasion plasmid. The gene (designated virB) was identified and its nucleotide sequence determined. No Ipa b or c was produced in the absence of an intact virB gene although lower levels of d were produced. The previously reported regulatory activity of the virF gene some 30 kb distance away was shown to act exclusively through virB. In contrast, the activation of the virG gene necessary for intercellular spread occurred directly by virF without the requirement for virB. This study thus ascribes a critical function to a previously recognized, but functionally undefined, virulence locus on the large invasion plasmid of S. flexneri. The virF gene appears to have a central role in activation of the 230 kb plasmid-encoded virulence genes.
有人发现，弗氏志贺氏菌质粒编码的侵袭相关抗原lpa b、c和d的表达在转录水平上受到一种33kD蛋白质的正向调控，该蛋白质由230kb侵袭质粒SalI片段B上先前确定的毒力相关区域1产生。该基因（命名为virB）已被鉴定并确定了其核苷酸序列。在没有完整virB基因的情况下，不产生Ipa b或c，尽管d的产生水平较低。先前报道的约30kb远处的virF基因的调控活性被证明仅通过virB起作用。相比之下，细胞间传播所必需的virG基因的激活直接由virF完成，无需virB。因此，本研究将一个先前已识别但功能未明的毒力位点赋予了关键功能，该位点位于弗氏志贺氏菌大型侵袭质粒上。virF基因似乎在激活230kb质粒编码的毒力基因中起核心作用。
