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首页> 外文期刊>Infection and immunity >Liposomes Recruit IpaC to the Shigella flexneri Type III Secretion Apparatus Needle as a Final Step in Secretion Induction
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Liposomes Recruit IpaC to the Shigella flexneri Type III Secretion Apparatus Needle as a Final Step in Secretion Induction

机译：脂质体向弗氏志贺氏菌III型分泌器械针招募IpaC作为分泌诱导的最后一步

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Shigella flexneri contact with enterocytes induces a burst of protein secretion via its type III secretion apparatus (TTSA) as an initial step in cellular invasion. We have previously reported that IpaD is positioned at the TTSA needle tip (M. Espina et al., Infect. Immuno. 74:4391-4400, 2006). From this position, IpaD senses small molecules in the environment to control the presentation of IpaB to the needle tip. This step occurs without type III secretion induction or IpaC recruitment to the S. flexneri surface. IpaC is then transported to the S. flexneri surface when target cell lipids are added, and this event presumably mimics host cell contact. Unlike IpaB mobilization, IpaC surface presentation is closely linked to secretion induction. This study demonstrates that sphingomyelin and cholesterol are key players in type III secretion induction and that they appear to interact with IpaB to elicit IpaC presentation at the TTSA needle tip. Furthermore, IpaB localization at the needle tip prior to membrane contact provides the optimal set of conditions for host cell invasion. Thus, the S. flexneri type III secretion system can be induced in a stepwise manner, with the first step being the stable association of IpaD with the needle tip, the second step being the sensing of small molecules by IpaD to mobilize IpaB to the tip, and the third step being the interaction of lipids with IpaB to induce IpaC localization at the needle tip concomitant with translocon insertion into the host membrane and type III secretion induction.
机译：弗氏志贺氏菌与肠细胞的接触通过其III型分泌装置（TTSA）诱导蛋白质分泌爆发，这是细胞入侵的第一步。我们以前已经报道过，IpaD位于TTSA针尖上（M. Espina等人，Infect。Immuno。74：4391-4400，2006）。从这个位置，IpaD可以感知环境中的小分子，以控制IpaB向针尖的呈现。在没有III型分泌诱导或IpaC募集到 S的情况下进行此步骤。 flexneri 表面。然后将IpaC传输到 S。当添加靶细胞脂质时，弗氏菌表面会出现，这种事件可能模拟宿主细胞接触。与IpaB动员不同，IpaC表面呈递与分泌诱导密切相关。这项研究表明鞘磷脂和胆固醇是III型分泌诱导的关键因素，并且它们似乎与IpaB相互作用以引起TTSA针尖的IpaC呈递。此外，IpaB在膜接触之前在针尖的定位为宿主细胞入侵提供了最佳条件。因此， S。可以逐步诱导flexneri型III型分泌系统，第一步是IpaD与针尖的稳定结合，第二步是IpaD感测小分子以将IpaB动员到尖端，第三步是脂质与IpaB相互作用，诱导IpaC定位在针尖，并与translocon插入宿主膜并诱导III型分泌。

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