Svinarich D M, Palchaudhuri S
Department of Molecular Biology and Genetics, Wayne State University School of Medicine, Detroit, MI 48201.
J Diarrhoeal Dis Res. 1992 Sep;10(3):139-45.
The regulation of Shiga toxin expression in a clinical isolate of S. dysenteriae 1 by the Fe-Fur (Iron-ferric uptake regulatory protein) repressor complex was investigated. The presence of an endogenous Fur repressor protein capable of binding to either a Fur binding consensus sequence or the regulatory region of SLT-1A was determined in toxinogenic strains of S. dysenteriae. Plasmid constructs bearing Fur binding sites fused to readily assayable reporter genes were used. Plasmid pSC27.1 contains a 21 bp synthetic oligonucleotide Fur protein binding consensus sequence located upstream to the gene for beta-galactosidase. Plasmid pSC105 contains the regulatory sequences of Shiga-like toxin-1A located upstream to the gene for alkaline phosphatase. In an analogous fashion to Shiga toxin regulation in S. dysenteriae 1, transformants bearing either pSC27.1 or pSC105 plasmid DNA were repressed in gene product expression when grown in minimal medium supplemented with iron. Conversely, transformants were de-repressed when grown under iron limiting conditions. These data suggest the presence of Fe-Fur mediated regulation of toxinogenesis in clinical isolates of S. dysenteriae.
研究了铁-铁摄取调节蛋白（Fe-Fur）阻遏复合物对痢疾志贺氏菌1临床分离株中志贺毒素表达的调控。在产毒素的痢疾志贺氏菌菌株中，确定了存在一种能够与Fur结合共有序列或SLT-1A调控区域结合的内源性Fur阻遏蛋白。使用了携带与易于检测的报告基因融合的Fur结合位点的质粒构建体。质粒pSC27.1在β-半乳糖苷酶基因上游含有一个21 bp的合成寡核苷酸Fur蛋白结合共有序列。质粒pSC105在碱性磷酸酶基因上游含有志贺样毒素-1A的调控序列。与痢疾志贺氏菌1中志贺毒素的调控方式类似，携带pSC27.1或pSC105质粒DNA的转化体在补充铁的基本培养基中生长时，基因产物表达受到抑制。相反，在铁限制条件下生长时，转化体被去抑制。这些数据表明在痢疾志贺氏菌临床分离株中存在Fe-Fur介导的毒素生成调控。
