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Palmitoylation of the influenza A virus M2 protein

R J Sugrue1, R B Belshe, A J Hay

  • 1Virology Division, National Institute for Medical Research, Mill Hill, London, United Kingdom.

Virology
|November 1, 1990
PubMed

Insights

Influenza A virus M2 proteins are palmitoylated via a thioester linkage to cysteine. This palmitoylation site, cysteine 50, is replaced by phenylalanine in equine H3N8 viruses, preventing acylation.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Influenza A virus M2 protein is a vital ion channel.
  • Post-translational modifications of viral proteins influence their function and pathogenesis.
  • Palmitoylation is a lipid modification that can affect protein localization and activity.

Purpose of the Study:

  • To investigate the palmitoylation of influenza A virus M2 proteins.
  • To identify the site and nature of palmitate attachment to M2.
  • To explore variations in M2 palmitoylation across different influenza A subtypes.

Main Methods:

  • Analysis of M2 proteins from various influenza A virus subtypes.
  • Treatment with reducing agents and hydroxylamine to assess thioester linkage.
  • Site-directed mutagenesis to investigate cysteine 50's role.

Main Results:

  • M2 proteins from multiple influenza A virus subtypes were found to be palmitoylated.
  • Palmitate removal by reduction and hydroxylamine suggests a thioester linkage to cysteine.
  • Equine H3N8 influenza A viruses showed absent palmitoylation, correlating with Cys50-Phe substitution.

Conclusions:

  • Influenza A virus M2 protein undergoes palmitoylation through a thioester linkage to cysteine.
  • Cysteine 50 is identified as the primary site of palmitoylation.
  • Substitution of Cys50 with phenylalanine in equine H3N8 viruses abrogates M2 palmitoylation.

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