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An infection-induced RhoB-Beclin 1-Hsp90 complex enhances clearance of uropathogenic Escherichia coli
Nature Communications ( IF 14.7 ) Pub Date : 2021-05-10 , DOI: 10.1038/s41467-021-22726-8
Chunhui Miao 1 , Mingyu Yu 1 , Geng Pei 1 , Zhenyi Ma 2 , Lisong Zhang 3 , Jianming Yang 1 , Junqiang Lv 1 , Zhi-Song Zhang 3 , Evan T Keller 4 , Zhi Yao 1, 5 , Quan Wang 1
Affiliation  

Host cells use several anti-bacterial pathways to defend against pathogens. Here, using a uropathogenic Escherichia coli (UPEC) infection model, we demonstrate that bacterial infection upregulates RhoB, which subsequently promotes intracellular bacteria clearance by inducing LC3 lipidation and autophagosome formation. RhoB binds with Beclin 1 through its residues at 118 to 140 and the Beclin 1 CCD domain, with RhoB Arg133 being the key binding residue. Binding of RhoB to Beclin 1 enhances the Hsp90-Beclin 1 interaction, preventing Beclin 1 degradation. RhoB also directly interacts with Hsp90, maintaining RhoB levels. UPEC infections increase RhoB, Beclin 1 and LC3 levels in bladder epithelium in vivo, whereas Beclin 1 and LC3 levels as well as UPEC clearance are substantially reduced in RhoB+/− and RhoB−/− mice upon infection. We conclude that when stimulated by UPEC infections, host cells promote UPEC clearance through the RhoB-Beclin 1-HSP90 complex, indicating RhoB may be a useful target when developing UPEC treatment strategies.



中文翻译:

感染诱导的 RhoB-Beclin 1-Hsp90 复合物可增强对尿路致病性大肠杆菌的清除

宿主细胞使用几种抗菌途径来防御病原体。在这里,使用尿路致病性大肠杆菌(UPEC) 感染模型,我们证明细菌感染上调 RhoB,其随后通过诱导 LC3 脂化和自噬体形成来促进细胞内细菌清除。RhoB 通过其 118 至 140 处的残基和 Beclin 1 CCD 结构域与 Beclin 1 结合,其中 RhoB Arg133 是关键的结合残基。RhoB 与 Beclin 1 的结合增强了 Hsp90-Beclin 1 的相互作用,防止了 Beclin 1 的降解。RhoB 还直接与 Hsp90 相互作用,维持 RhoB 水平。UPEC感染增加RhoB的,自噬基因Beclin 1和LC3水平在膀胱上皮体内,而自噬基因Beclin 1和LC3水平以及间隙UPEC在基本上减少RhoB的+/-RhoB -/-小鼠感染后。我们得出结论,当受到 UPEC 感染的刺激时,宿主细胞通过 RhoB-Beclin 1-HSP90 复合物促进 UPEC 清除,这表明 RhoB 在开发 UPEC 治疗策略时可能是一个有用的目标。

更新日期:2021-05-10
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