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An infection-induced RhoB-Beclin 1-Hsp90 complex enhances clearance of uropathogenic Escherichia coli

Author

Listed:
  • Chunhui Miao

    (Tianjin Medical University)

  • Mingyu Yu

    (Tianjin Medical University)

  • Geng Pei

    (Tianjin Medical University)

  • Zhenyi Ma

    (Tianjin Medical University)

  • Lisong Zhang

    (Nankai University)

  • Jianming Yang

    (Tianjin Medical University)

  • Junqiang Lv

    (Tianjin Medical University)

  • Zhi-Song Zhang

    (Nankai University)

  • Evan T. Keller

    (University of Michigan)

  • Zhi Yao

    (Tianjin Medical University
    Tianjin Medical University)

  • Quan Wang

    (Tianjin Medical University)

Abstract

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.

Suggested Citation

  • Chunhui Miao & Mingyu Yu & Geng Pei & Zhenyi Ma & Lisong Zhang & Jianming Yang & Junqiang Lv & Zhi-Song Zhang & Evan T. Keller & Zhi Yao & Quan Wang, 2021. "An infection-induced RhoB-Beclin 1-Hsp90 complex enhances clearance of uropathogenic Escherichia coli," Nature Communications, Nature, vol. 12(1), pages 1-15, December.
  • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22726-8
    DOI: 10.1038/s41467-021-22726-8
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