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首页> 外文期刊>Biology Open >The bacterial and cellular determinants controlling the recruitment of mTOR to the Salmonella-containing vacuole
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The bacterial and cellular determinants controlling the recruitment of mTOR to the Salmonella-containing vacuole

机译：控制mTOR募集到含沙门氏菌液泡的细菌和细胞决定因素

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Bacterial invasion results in the rapid induction of an acute state of cytosolic amino acid (AA) starvation, provoked by host membrane damage. Bacteria-induced AA starvation, in turn, down-regulates mTOR signaling while triggering autophagy and the integrated stress response pathway dependent on GCN2, eIF2α and ATF3. In Salmonella -infected cells, we now demonstrate that the host AA starvation response program depended on the Salmonella pathogenicity island (SPI)-1, the activity of which was required to damage the Salmonella -containing vacuole (SCV) in the early stage of infection. At a later stage (3–4?hour post-infection), the progressive recruitment of mTOR to the surface of the SCV appeared to be independent of the activity of SPI-2 and of SCV positioning in the cell. Instead, mTOR localization to the SCV required the activity of host AA transporters SLC1A5, SLC3A2 and SLC7A5, resulting in bacterial escape from autophagy. These results expand our understanding of the mechanisms underlying the AA starvation response in Salmonella -infected cells.
机译：细菌入侵导致急性诱导的细胞溶质氨基酸（AA）饥饿的急性状态，这是由宿主膜损伤引起的。反过来，细菌引起的AA饥饿会下调mTOR信号传导，同时触发自噬和依赖于GCN2，eIF2α和ATF3的整合应激反应途径。在沙门氏菌感染的细胞中，我们现在证明宿主AA饥饿反应程序依赖于沙门氏菌致病岛（SPI）-1，沙门氏菌致病岛（SPI）-1的活性在感染早期需要破坏含沙门氏菌的液泡（SCV） 。在后期（感染后3-4小时），mTOR逐渐募集到SCV表面似乎与SPI-2的活性和SCV在细胞中的定位无关。相反，将mTOR定位到SCV需要宿主AA转运蛋白SLC1A5，SLC3A2和SLC7A5的活性，从而导致细菌从自噬中逸出。这些结果扩展了我们对沙门氏菌感染细胞中AA饥饿反应潜在机制的理解。

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