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首页> 外文期刊>Infection and immunity >IpaD of Shigella flexneri Is Independently Required for Regulation of Ipa Protein Secretion and Efficient Insertion of IpaB and IpaC into Host Membranes
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IpaD of Shigella flexneri Is Independently Required for Regulation of Ipa Protein Secretion and Efficient Insertion of IpaB and IpaC into Host Membranes

机译：弗氏志贺氏菌的IpaD是调节Ipa蛋白分泌以及将IpaB和​​IpaC有效插入宿主膜的独立必需的。

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Shigella flexneri causes human dysentery after invading the cells of the colonic epithelium. The best-studied effectors of Shigella entry into colonocytes are the invasion plasmid antigens IpaC and IpaB. These proteins are exported via a type III secretion system (TTSS) to form a pore in the host membrane that may allow the translocation of other effectors into the host cytoplasm. TTSS-mediated secretion of IpaD is also required for translocation pore formation, bacterial invasion, and virulence, but the mechanistic role of this protein is unclear. IpaD is also known to be involved in controlling Ipa protein secretion, but here it is shown that this activity can be separated from its requirement for cellular invasion. Amino acids 40 to 120 of IpaD are not essential for IpaD-dependent invasion; however, deletions in this region still lead to constitutive IpaB/IpaC secretion. Meanwhile, a central deletion causes only a partial loss of control of Ipa secretion but completely eliminates IpaD's invasion function, indicating that IpaD's role in invasion is not a direct outcome of its ability to control Ipa secretion. As shigellae expressing ipaD N-terminal deletion mutations have reduced contact-mediated hemolysis activity and are less efficient at introducing IpaB and IpaC into erythrocyte membranes, it is possible that IpaD is responsible for insertion of IpaB/IpaC pores into target cell membranes. While efficient insertion of IpaB/IpaC pores is needed for optimal invasion efficiency, it may be especially important for Ipa-dependent membrane disruption and thus for efficient vacuolar escape and intercellular spread.
机译：弗氏志贺氏菌在侵袭结肠上皮细胞后引起人痢疾。研究最多的志贺氏菌进入结肠细胞的效应子是入侵质粒抗原IpaC和IpaB。这些蛋白质通过III型分泌系统（TTSS）输出，在宿主膜上形成孔，这可能使其他效应子易位到宿主细胞质中。 TTSS介导的IpaD分泌对于易位孔形成，细菌入侵和毒力也是必需的，但该蛋白的机械作用尚不清楚。还已知IpaD参与控制Ipa蛋白的分泌，但此处表明该活性可以与细胞入侵的需要分开。 IpaD的40至120位氨基酸对于IpaD依赖的入侵不是必需的。然而，该区域的缺失仍然导致组成型IpaB / IpaC分泌。同时，中央缺失仅引起对Ipa分泌的控制的部分丧失，但完全消除了IpaD的侵袭功能，表明IpaD在侵袭中的作用不是其控制Ipa分泌能力的直接结果。由于志贺氏菌表达 ipaD N端缺失突变具有降低的接触介导的溶血活性，并且在将IpaB和​​IpaC引入红细胞膜中的效率较低，因此IpaD可能负责IpaB / IpaC孔的插入进入靶细胞膜。虽然需要IpaB / IpaC孔的有效插入来获得最佳的侵袭效率，但对于依赖Ipa的膜破坏，从而对于有效的液泡逃逸和细胞间扩散而言，这可能尤其重要。

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