Acylation and cholesterol binding are not required for targeting of influenza A virus M2 protein to the hemagglutinin-defined budozone

FEBS Lett. 2014 Mar 18;588(6):1031-6. doi: 10.1016/j.febslet.2014.02.014. Epub 2014 Feb 20.

Abstract

Influenza virus assembles in the budozone, a cholesterol-/sphingolipid-enriched ("raft") domain at the apical plasma membrane, organized by hemagglutinin (HA). The viral protein M2 localizes to the budozone edge for virus particle scission. This was proposed to depend on acylation and cholesterol binding. We show that M2-GFP without these motifs is still transported apically in polarized cells. Employing FRET, we determined that clustering between HA and M2 is reduced upon disruption of HA's raft-association features (acylation, transmembranous VIL motif), but remains unchanged with M2 lacking acylation and/or cholesterol-binding sites. The motifs are thus irrelevant for M2 targeting in cells.

Keywords: Apical transport; Hemagglutinin; Influenza virus; M2; Palmitoylation; Raft localization.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acylation
  • Animals
  • CHO Cells
  • Cell Polarity
  • Cholesterol / metabolism*
  • Cricetinae
  • Cricetulus
  • Dogs
  • Hemagglutinin Glycoproteins, Influenza Virus / metabolism
  • Influenza A virus / physiology*
  • Madin Darby Canine Kidney Cells
  • Membrane Microdomains / metabolism
  • Membrane Microdomains / virology*
  • Protein Binding
  • Protein Processing, Post-Translational
  • Protein Transport
  • Viral Matrix Proteins / metabolism*
  • Virus Assembly

Substances

  • Hemagglutinin Glycoproteins, Influenza Virus
  • M2 protein, Influenza A virus
  • Viral Matrix Proteins
  • Cholesterol