Many bacterial small RNAs (sRNAs) efficiently inhibit translation of target mRNAs by forming a duplex that sequesters the Shine‐Dalgarno (SD) sequence or start codon and prevents formation of the translation initiation complex. There are a growing number of examples of sRNA–mRNA binding interactions distant from the SD region, but how these mediate translational regulation remains unclear. Our previous work in Escherichia coli and Salmonella identified a mechanism of translational repression of manY mRNA by the sRNA SgrS through a binding interaction upstream of the manY SD. Here, we report that SgrS forms a duplex with a uridine‐rich translation‐enhancing element in the manY 5ʹ untranslated region. Notably, we show that the enhancer is ribosome‐dependent and that the small ribosomal subunit protein S1 interacts with the enhancer to promote translation of manY. In collaboration with the chaperone protein Hfq, SgrS interferes with the interaction between the translation enhancer and ribosomal protein S1 to repress translation of manY mRNA. Since bacterial translation is often modulated by enhancer‐like elements upstream of the SD, sRNA‐mediated enhancer silencing could be a common mode of gene regulation.

中文翻译：

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远距离翻译抑制：小 RNA SgrS 沉默核糖体蛋白 S1 依赖性增强子。

许多细菌小 RNA (sRNA) 通过形成双链体来隔离 Shine-Dalgarno (SD) 序列或起始密码子并阻止翻译起始复合物的形成，从而有效抑制目标 mRNA 的翻译。远离 SD 区域的 sRNA-mRNA 结合相互作用的例子越来越多，但这些相互作用如何介导翻译调节仍不清楚。我们以前的工作中大肠杆菌和沙门氏菌鉴定的翻译抑制的机制许多由的sRNA的SGR的mRNA通过的结合相互作用上游许多SD。在这里，我们报告的SGR形成复式的丰富尿苷翻译增强元件多5ʹ 未翻译的地区。值得注意的是，我们表明增强子是核糖体依赖性的，并且小核糖体亚基蛋白 S1 与增强子相互作用以促进manY 的翻译。SgrS 与伴侣蛋白 Hfq 合作，干扰翻译增强子和核糖体蛋白 S1 之间的相互作用，以抑制manY mRNA 的翻译。由于细菌翻译通常由 SD 上游的增强子样元件调节，sRNA 介导的增强子沉默可能是基因调控的常见模式。