Expression of the antiviral protein MxA in cells transiently perturbs endocytosis

Shashidhar S Jatiani1, Rohit Mittal

  • 1Department of Biological Sciences, Tata Institute of Fundamental Research, Homi Bhabha Road, Colaba, Mumbai 400 005, India.

Insights

MxA protein, an antiviral defense, temporarily disrupts cellular trafficking and transferrin recycling. This effect is linked to MxA

Area of Science:

  • Cellular Biology
  • Virology
  • Protein Trafficking

Background:

  • MxA is an interferon-induced protein with known antiviral functions.
  • Viral replication depends on host cell trafficking machinery.
  • Understanding MxA's cellular interactions is key to its antiviral mechanisms.

Purpose of the Study:

  • To investigate the effect of MxA overexpression on cellular trafficking pathways.
  • To elucidate the mechanism by which MxA influences endocytosis and recycling.
  • To identify potential protein interactions of MxA involved in trafficking.

Main Methods:

  • Overexpression of MxA protein in cultured cells.
  • Tracking of internalized transferrin to assess endocytic and recycling functions.
  • Analysis of MxA protein levels and trafficking perturbation over time.
  • Co-immunoprecipitation assays to detect MxA-dynamin association.

Main Results:

  • MxA overexpression transiently perturbs endocytic trafficking, causing transferrin accumulation.
  • The maximal effect on transferrin endocytosis occurs 5-6 hours post-transfection.
  • Transferrin recycling is blocked, but the trafficking perturbation subsides by 12 hours despite sustained MxA levels.
  • MxA physically associates with the endocytic protein dynamin.

Conclusions:

  • MxA influences cellular trafficking, specifically endocytosis and recycling.
  • The interaction between MxA and dynamin likely mediates the observed effects on transferrin trafficking.
  • This study reveals a novel role for MxA in modulating host cell transport processes.