菌肺炎效应物SidL (Lpg0437) 的晶体结构与其元效应物Lega11 (Lpg0436) 的复合体
Dominik A Machtens1, Carissa A Hutchison2, Ashley M Stein3
1Institute for Biophysical Chemistry, Hannover Medical School, Carl-Neuberg-Straße 1, 30625 Hannover, Germany.
bioRxiv : the preprint server for biology
|November 24, 2025
概括
肺炎杆菌使用LegaA11这样的元效应器来控制宿主细胞. LegA11直接结合并抑制SidL,一种阻止宿主mRNA转换的蛋白质,从而有助于细菌的复制.
科学领域:
- 微生物学 微生物学
- 分子生物学分子生物学
- 结构生物学 结构生物学
背景情况:
- 肺炎菌 (Legionella pneumophila) 通过注射效应蛋白到宿主细胞中引起军团士兵病.
- 超效因子调节其他效因子,影响宿主细胞的过程,如mRNA转化.
- 乐格A11是SidL的疑似metaeffector,这是宿主mRNA翻译的抑制剂.
研究的目的:
- 阐明LegA11调节SidL的分子机制.
- 为了确定LegA11-SidL相互作用的结构基础.
- 确认LegA11作为抑制宿主mRNA转化中的元效应者的作用.
主要方法:
- 进行X射线晶体学以确定SidL-LegA11复杂结构.
- 异热定位热量计,以量化结合亲和力.
- 在体外翻译试验和局部定向突变发生,以评估功能影响.
主要成果:
- 在SidL和LegA11之间的高亲缘性1:1复合体在结构上具有特征 (2.4 Å分辨率).
- 莱加A11完全抑制了SidL对体外mRNA翻译的抑制作用.
- 接口残留物的突变性取消了Lega11的元效应器功能,证实了直接相互作用.
结论:
- LegA11是一种真正的元效应器,直接结合并抑制SidL.
- 这种LegA11-SidL相互作用对于抑制宿主mRNA转化由Legionella pneumophila至关重要.
- 这项研究提供了对感染期间细菌效应器调节的结构和功能见解.
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