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首页> 外文期刊>Nature >A Salmonella protein antagonizes Rac-1 and Cdc42 to mediate host-cell recovery after bacterial invasion
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A Salmonella protein antagonizes Rac-1 and Cdc42 to mediate host-cell recovery after bacterial invasion

机译：沙门氏菌蛋白拮抗Rac-1和Cdc42以介导细菌入侵后宿主细胞的恢复

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摘要

An essential feature of the bacterial pathogen Salmonella spp. is its ability to enter cells that are normally non-phagocytic, such as those of the intestinal epithelium. The bacterium achieves entry by delivering effector proteins into the host-cell cytosol by means of a specialized protein-secretion system (termed type Ⅲ), which causes reorganization of the cell's actin cytoskeleton and ruffling of its membrane. One of the bacterial effectors that stimulates these cellular responses is SopE, which acts as a guanyl-nucleo-tide-exchange factor on Rho GTPase proteins such as Cdc42 and Rac (ref. 5). As the actin-cytoskeleton reorganization induced by Salmonella is reversible and short-lived, infected cells regain their normal architecture after bacterial internalization. We show here that the S. Typhimurium effector protein SptP, which is delivered to the host-cell cytosol by the type-Ⅲ secretion system, is directly responsible for the reversal of the actin cytoskeletal changes induced by the bacterium. SptP exerts this function by acting as a GTPase-activating protein (GAP) for Rac-1 and Cdc42.
机译：细菌病原体沙门氏菌的一个基本特征。它进入正常非吞噬细胞（例如肠上皮细胞）的能力。细菌通过特殊的蛋白质分泌系统（称为Ⅲ型）将效应蛋白传递到宿主细胞的胞质溶胶中而进入，从而引起细胞肌动蛋白细胞骨架的重组和膜的起伏。刺激这些细胞反应的细菌效应物之一是SopE，它充当Rho GTPase蛋白（如Cdc42和Rac）上的鸟苷酸-核苷酸交换因子（参考文献5）。由于沙门氏菌诱导的肌动蛋白-细胞骨架重组是可逆的且寿命短，因此细菌内化后，受感染的细胞可恢复其正常结构。我们在这里显示，鼠伤寒沙门氏菌效应蛋白SptP通过Ⅲ型分泌系统传递到宿主细胞的胞质溶胶中，直接导致了细菌诱导的肌动蛋白细胞骨架变化的逆转。 SptP通过充当Rac-1和Cdc42的GTPase激活蛋白（GAP）发挥此功能。

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  • 来源
    《Nature》 |1999年第6750期|p.293-297|共5页
  • 作者

    Y Fu; J E Galan;

  • 作者单位
  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 自然科学总论;
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