Badger J L, Miller V L
Department of Microbiology and Molecular Genetics, University of California, Los Angeles 90095, USA.
J Bacteriol. 1998 Feb;180(4):793-800. doi: 10.1128/JB.180.4.793-800.1998.
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.
小肠结肠炎耶尔森菌的inv基因编码主要侵袭因子侵袭素,此前已证明该因子在感染初期至关重要。inv的表达受生长阶段和温度影响,在23℃下指数后期至稳定前期达到最大值。此外,小肠结肠炎耶尔森菌的运动性受温度调节。小肠结肠炎耶尔森菌细胞在较低温度(30℃或更低)下生长时具有运动性,而在37℃下生长的细菌则不具有运动性。本研究旨在确定inv表达温度调节的分子基础。分离出两个突变体,它们在23℃下生长时侵袭素表达均显著降低,但运动性增强。第一个突变体(JB1A8v)是由于mTn5Km随机插入uvrC基因所致。uvrC突变体JB1A8v的inv显著降低,而fleB(编码鞭毛蛋白)表达增加。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。第二个调节突变体JB16v是由于靶向插入一个与sspA相似的位点所致,在大肠杆菌中sspA编码一个稳定期调节因子。克隆了大肠杆菌的sspA基因,并在两个调节突变体中进行互补检测。结果表明,大肠杆菌的sspA恢复了uvrC突变体和sspA突变体中的侵袭素表达。此外,互补克隆降低了这些突变体中的鞭毛蛋白水平。