SARS-CoV-2 ORF10 impairs cilia by enhancing CUL2ZYG11B activity

J Cell Biol. 2022 Jul 4;221(7):e202108015. doi: 10.1083/jcb.202108015. Epub 2022 Jun 8.

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal pathogen of the ongoing global pandemic of coronavirus disease 2019 (COVID-19). Loss of smell and taste are symptoms of COVID-19, and may be related to cilia dysfunction. Here, we found that the SARS-CoV-2 ORF10 increases the overall E3 ligase activity of the CUL2ZYG11B complex by interacting with ZYG11B. Enhanced CUL2ZYG11B activity by ORF10 causes increased ubiquitination and subsequent proteasome-mediated degradation of an intraflagellar transport (IFT) complex B protein, IFT46, thereby impairing both cilia biogenesis and maintenance. Further, we show that exposure of the respiratory tract of hACE2 mice to SARS-CoV-2 or SARS-CoV-2 ORF10 alone results in cilia-dysfunction-related phenotypes, and the ORF10 expression in primary human nasal epithelial cells (HNECs) also caused a rapid loss of the ciliary layer. Our study demonstrates how SARS-CoV-2 ORF10 hijacks CUL2ZYG11B to eliminate IFT46 and leads to cilia dysfunction, thereby offering a powerful etiopathological explanation for how SARS-CoV-2 causes multiple cilia-dysfunction-related symptoms specific to COVID-19.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cells, Cultured
  • Cilia* / metabolism
  • Cilia* / pathology
  • Cytoskeletal Proteins
  • Epithelial Cells / metabolism
  • Epithelial Cells / virology
  • Humans
  • Mice
  • SARS-CoV-2* / pathogenicity
  • Smell
  • Ubiquitin-Protein Ligases* / metabolism

Substances

  • Cytoskeletal Proteins
  • IFT46 protein, mouse
  • Ubiquitin-Protein Ligases