...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Expression of the Listeria monocytogenes EGD inlA and inlB genes, whose products mediate bacterial entry into tissue culture cell lines, by PrfA-dependent and -independent mechanisms.
【24h】

Expression of the Listeria monocytogenes EGD inlA and inlB genes, whose products mediate bacterial entry into tissue culture cell lines, by PrfA-dependent and -independent mechanisms.

机译：单核细胞增生李斯特菌EGD inlA和inlB基因的表达，其产物通过PrfA依赖性和非依赖性机制介导细菌进入组织培养细胞系。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Internalization of Listeria monocytogenes into nonphagocytic cell lines in vitro requires the products of the inlAB locus (J.-L. Gaillard, P. Berche, C. Frehel, E. Gouin, and P. Cossart, Cell 65:1127-1141, 1991). By generating isogenic mutants with a chromosomal in-frame deletion in either inlA or inlB, we have identified InlA and InlB as surface-bound proteins of L. monocytogenes with molecular weights of 88,000 and 65,000, respectively. These results were obtained with monoclonal antibodies raised against either protein and corroborated by N-terminal end sequencing of InlA and InlB. By immunoblot analysis, the production of both polypeptides was found to be strongly dependent on growth temperature and, particularly for InlB, on the presence of the PrfA regulator protein. Expression of InlA was not strictly dependent on the presence of the PrfA regulator protein. Transcription analysis of the inlAB locus revealed that the inlA gene was transcribed by several promoters, of which only one is PrfA dependent. This PrfA-dependent inlA promoter, which contains two base substitutions within its putative PrfA DNA-binding palindrome, is responsible for transcription of both inlA and inlB genes. A hitherto unrecognized promoter located 51 bp upstream of the GTG start codon of the inlB gene was also detected. Hence, inlA and inlB are transcribed both individually and in an operon by PrfA-dependent and -independent mechanisms. Tissue culture invasion assays employing various epithelial cell lines demonstrated that both InlA and InlB are required for invasion. In vivo studies using the mouse infection model revealed that both internalin mutants were attenuated for virulence.
机译：在体外将单核细胞增生李斯特菌内化到非吞噬细胞系中需要inlAB基因座的产物（J.-L. Gaillard，P.Berche，C.Frehel，E.Gouin和P.Cossart，Cell 65：1127-1141，1991 ）。通过在inlA或inlB中产生具有染色体内读框缺失的等基因突变体，我们已将InlA和InlB鉴定为单核细胞增生李斯特氏菌的表面结合蛋白，分子量分别为88,000和65,000。这些结果是通过针对任一蛋白质产生的单克隆抗体获得的，并通过InlA和InlB的N末端测序证实了这一结果。通过免疫印迹分析，发现两种多肽的产生都强烈依赖于生长温度，尤其是对于InlB，依赖于PrfA调节蛋白的存在。 InlA的表达并不严格取决于PrfA调节蛋白的存在。对inlAB基因座的转录分析表明，inlA基因被多个启动子转录，其中只有一个是PrfA依赖性的。这种依赖PrfA的inlA启动子在其假定的PrfA DNA结合回文中包含两个碱基取代，负责inlA和inlB基因的转录。还检测到迄今尚未发现的启动子，该启动子位于inlB基因的GTG起始密码子上游51 bp。因此，通过依赖于PrfA和独立于PrfA的机制，inlA和inlB既可以单独转录也可以在操纵子中转录。采用各种上皮细胞系的组织培养物侵袭测定表明，InlA和InlB都是侵袭所必需的。使用小鼠感染模型的体内研究表明，两个internalin突变体的毒力均减弱。

著录项

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