首页> 外文学位 >Temperature regulation of inv by RovA, YmoA and H-NS in Yersinia enterocolitica.
【24h】

Temperature regulation of inv by RovA, YmoA and H-NS in Yersinia enterocolitica.

机译:RovA,YmoA和H-NS在小肠结肠炎耶尔森菌中对inv的温度调节。

获取原文
获取原文并翻译 | 示例

摘要

Invasin is an outer membrane protein found in Y. enterocolitica and Y. pseudotuberculosis that is sufficient to mediate invasion of host cells. Invasin is encoded by the inv gene and is maximally expressed during in vitro growth in late exponential to early stationary phase and responds to changes in temperature and pH of the growth media. Three proteins that have been shown to regulate inv transcription are RovA, which is required for inv activation and YmoA and H-NS, which are involved in the repression of inv. RovA and H-NS specifically bind the inv promoter and preferentially interact with the same segments of the promoter. RovA and H-NS are able to displace one another from the inv promoter in vitro, suggesting that RovA and H-NS are directly competing for the same binding sites. Removal of the H-NS/RovA binding sites from the inv promoter results in inv activation independent of RovA, suggesting that RovA is acting as a derepressor. While YmoA is required for repression of inv, it does not specifically recognize the inv promoter. YmoA negatively affects the expression of inv through direct interaction with H-NS, with H-NS supplying the binding specificity for the complex. Levels of hns and ymoA transcripts are similar between 26°C and 37°C suggesting that the H-NS/YmoA repression complex is present at both temperatures, while the levels of rovA are low at 37°C and high at 26°C. Exogenous expression of RovA at 37°C results in activation of inv transcription suggesting that levels of RovA are critical for overcoming repression of inv transcription. Data presented here support a model of inv regulation where the level of RovA within the cell governs inv expression. As RovA levels increase, RovA can successfully compete for binding to the inv promoter with the H-NS/YmoA complex resulting in derepression of inv transcription.
机译:入侵素是在小肠结肠炎耶尔森氏菌和假结核耶尔森氏菌中发现的一种外膜蛋白,足以介导宿主细胞的侵袭。 Invasin由inv基因编码,并在体外生长过程中在指数晚期至固定早期阶段最大程度表达,并响应生长培养基的温度和pH值变化。已经显示出可调节inv转录的三种蛋白质是RovA(这是inv激活所必需的)和YmoA和H-NS,它们参与inv的抑制。 RovA和H-NS特异性结合inv启动子,并优先与启动子的相同片段相互作用。 RovA和H-NS能够在体外从inv启动子中相互置换,这表明RovA和H-NS直接竞争相同的结合位点。从inv启动子上去除H-NS / RovA结合位点会导致inv激活独立于RovA,这表明RovA充当了抑制因子。尽管YmoA是抑制inv所必需的,但它并不特异性识别inv启动子。 YmoA通过与H-NS直接相互作用而负面影响inv的表达,其中H-NS提供了复合物的结合特异性。 hns和ymoA转录本的水平在26°C和37°C之间相似,这表明在两种温度下均存在H-NS / YmoA抑制复合物,而rovA的水平在37°C时较低,而在26°C时较高。 RovA在37°C的外源表达导致inv转录的激活,这表明RovA的水平对于克服inv转录的抑制至关重要。此处提供的数据支持inv调节模型,其中细胞内RovA的水平决定了inv表达。随着RovA水平的提高,RovA可以成功竞争与H-NS / YmoA复合物与inv启动子的结合,从而导致inv转录的抑制。

著录项

  • 作者

    Ellison, Damon William.;

  • 作者单位

    Washington University in St. Louis.;

  • 授予单位 Washington University in St. Louis.;
  • 学科 Biology Molecular.; Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 115 p.
  • 总页数 115
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 分子遗传学;微生物学;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号