Expression of invasin and motility are coordinately regulated in Yersinia enterocolitica
Expression of invasin and motility are coordinately regulated in Yersinia enterocolitica
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DOI：
10.1128/jb.180.4.793-800.1998
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发表时间：
1998-02-01
影响因子：
3.2
通讯作者：
Miller, VL
中科院分区：
文献类型：
--
作者：
Badger, JL;Miller, VL
小肠结肠炎耶尔森氏菌inv基因编码主要侵袭因子invasin，其先前已被证明在感染的初始阶段是关键的。inv的表达受生长期和温度的影响，在23 ℃时在指数生长后期-稳定期早期达到最大。此外，Y.小肠结肠炎是由温度调节的。Y.小肠结肠炎细胞在较低温度（30摄氏度或以下）下生长时是能动的，而在37摄氏度下生长的细菌是不能动的。本研究旨在确定inv表达的温度调节的分子基础。分离出两种突变体，它们均显示侵袭素表达显著降低，但在23 ℃下生长时运动过度。第一个突变体（JB 1A 8v）是将mTn 5 Km随机插入uvrC基因的结果。uvrC突变体JB 1A 8v表现出inv的显著降低和fleB（编码鞭毛蛋白）表达的增加。这些结果表明inv和鞭毛蛋白基因的表达在转录水平上是协调的。第二个调控突变体JB 16 v是在大肠杆菌中与sspA相似的基因座上定向插入的结果。coli编码一个稳定期调节因子。急诊coli sspA基因的克隆，并分析了在两个调节突变体中的互补性。确定E. coli sspA恢复了uvrC突变体和sspA突变体中侵袭素的表达。此外，互补克隆降低了这些突变体中的鞭毛蛋白水平。
The Yersinia enterocolitica inv gene encodes the primary invasion factor invasin, which has been previously shown to be critical in the initial stages of infection. The expression of inv is influenced by growth phase and temperature and is maximal during late exponential-early stationary phase at 23 degrees C. In addition, motility of Y. enterocolitica is regulated by temperature. Y. enterocolitica cells are motile when grown at lower temperatures (30 degrees C or below), while bacteria grown at 37 degrees C are nonmotile. This study was initiated to determine the molecular basis for the temperature regulation of inv expression. Two mutants were isolated that both showed a significant decrease in invasin expression but are hypermotile when grown at 23 degrees C. The first mutant (JB1A8v) was a result of a random mTn5Km insertion into the uvrC gene. The uvrC mutant JB1A8v demonstrated a significant decrease in inv and an increase in fleB (encodes flagellin) expression. These results suggest that expression of inv and flagellin genes is coordinated at the level of transcription. The second regulatory mutant, JB16v, was a result of a targeted insertion into a locus similar to sspA which in E. coli encodes a Stationary-phase regulator. The E. coli sspA gene was cloned and assayed for complementation in both of the regulatory mutants. It was determined that E. coli sspA restored invasin expression in both the uvrC mutant and the sspA mutant. In addition, the complementing clone decreased flagellin levels in these mutants.