Small RNAs (sRNAs) are essential virulent regulators in Salmonella typhimurium (STM). To explore the role of sRNA STnc150 in regulating STM virulence, we constructed a STnc150 deletion strain (ΔSTnc150) and its complementary strain (ΔSTnc150/C). Then, we compared their characteristics to their original parent strain experimentally, identified the target genes of STnc150 and determined the expression levels of target genes. The results showed that the ΔSTnc150 strain exhibited delayed biofilm formation, enhanced adhesion to macrophages, significantly reduced LD₅₀, increased liver and spleen viral loads and more vital pathological damaging ability than its parent and complementary strains. Further, bioinformatics combined with the bacterial dual plasmid reporter system confirmed that the bases 72–88 of STnc150 locating at the secondary stem-loop structure of the STnc150 are complementary with the bases 1–19 in the 5′-terminal of fimA mRNA of the type 1 fimbriae subunit. Western blot analysis showed that fimA protein level was increased in STnc150 strain compared with its parent and complementary strains. Together, this study suggested that STnc150 can down-regulate STM fimA expression at the translation level, which provided insights into the regulatory mechanisms of sRNAs in virulence of STM.

中文翻译：

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sRNA STnc150 通过靶向 fimA mRNA 参与鼠伤寒沙门氏菌的毒力调节

小 RNA (sRNA) 是鼠伤寒沙门氏菌(STM)中必不可少的毒力调节剂。为了探索 sRNA STnc150在调节 STM 毒力中的作用，我们构建了一个STnc150缺失菌株（Δ STnc150）及其互补菌株（Δ STnc150 /C）。然后，我们通过实验将它们的特性与其原始亲本菌株进行了比较，鉴定了STnc150的靶基因并确定了靶基因的表达水平。结果表明，ΔSTnc150菌株生物膜形成延迟，对巨噬细胞的粘附增强，LD ₅₀显着降低，增加了肝脏和脾脏的病毒载量和比其亲本和互补菌株更重要的病理破坏能力。此外，生物信息学与细菌质粒双重报道系统结合证实，碱基的72-88 STnc150定位在二次茎环结构STnc150与在5'末端的碱基1-19互补FIMA的mRNA的1 型菌毛亚基。蛋白质印迹分析表明，与其亲本和互补菌株相比，STnc150菌株中的fimA蛋白水平增加。总之，这项研究表明STnc150可以下调 STM fimA 在翻译水平上表达，这提供了对 sRNA 在 STM 毒力中的调节机制的见解。