内巨RIL-seq发现了沙门氏菌病毒性相关小RNAPINT的RNA对手
Hoda Kooshapour1,2, Gianluca Matera2, Elisa Venturini2
1Department of Microbiology, Biocenter, University of Würzburg, Würzburg D-97074, Germany.
Nucleic acids research
|December 22, 2025
概括
沙门氏菌的毒性依赖于小型调节性RNA (sRNA). 一项新的研究显示,InvS通过作为诱来对抗Pint,一种毒性调节剂,从而提供了对沙门氏菌细胞内感染控制的见解.
科学领域:
- 微生物学 微生物学
- 分子生物学分子生物学
- 细菌学 细菌学是一门学科.
背景情况:
- 沙门氏菌的毒性取决于SPI-1和SPI-2的病原性岛屿.
- 像Pint这样的Hfq依赖的小调节RNA (sRNA) 在转录后控制病毒性基因表达.
- 在宿主细胞入侵期间,Pint调节了SPI-1和SPI-2表达之间的切换.
研究的目的:
- 为了研究在沙门氏菌的细胞内感染期间Pint活动的反调节.
- 在巨细胞内绘制沙门氏菌的RNA互动组图,以确定新的调节相互作用.
- 阐明PinT介导的抑制缓解的机制.
主要方法:
- 优化了RIL-seq以映射感染巨细胞内的沙门氏菌中的RNA-RNA相互作用.
- 生物化学测试以确认RNA相互作用和调节功能.
- 遗传实验验证已识别的sRNA在病毒性基因调节中的作用.
主要成果:
- 在细胞内感染期间,RIL-seq为Hfq介导的相互作用提供了全面的视图.
- 3'端衍生的sRNA InvS被确定为Pint的直接负调节器.
- InvS充当诱,缓解PinT介导的抑制,并抑制MipA mRNA;PinT与InvS的相互作用缓解了这种抑制.
结论:
- 在沙门氏菌中发现了一对对抗性sRNAs,Pint和InvS.
- InvS使用诱机制来抵消Pint的监管活动.
- 这些发现揭示了在沙门氏菌毒性调节中进行转录后控制的新层.
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