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Influenza virus M2 protein modifies membrane permeability in E. coli cells

R Guinea1, L Carrasco

  • 1Centro de Biologia Molecular, CSIC-UAM, Universidad Autónoma de Madrid, Canto Blanco, Spain.

FEBS Letters
|May 2, 1994
PubMed

Insights

Influenza virus M2 protein, expressed in E. coli, disrupts bacterial cell membranes, increasing permeability. This viral ion channel activity causes rapid cell lysis, offering insights into membrane protein function.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Influenza virus M2 protein is an integral membrane protein.
  • M2 protein exhibits ion channel activity crucial for viral function.

Purpose of the Study:

  • To investigate the expression and functional consequences of influenza virus M2 protein in E. coli.
  • To characterize the impact of M2 protein on bacterial cell membrane permeability and integrity.

Main Methods:

  • Inducible expression of influenza M2 protein in BL21(DE3) pLysS E. coli.
  • Assessing cell viability and lysis post-induction with IPTG.
  • Measuring membrane permeability to hydrophilic molecules like ONPG and uridine.

Main Results:

  • M2 protein expression led to rapid lysis of E. coli cells.
  • Increased membrane permeability to ONPG, uridine, and impermeant translation inhibitors was observed.
  • Bacterial behavior mirrored that of other viral proteins (poliovirus 3A, Semliki Forest virus 6K).

Conclusions:

  • Influenza M2 protein possesses functional ion channel activity in bacterial systems.
  • M2 protein expression compromises bacterial membrane integrity, leading to cell death.
  • The study provides a bacterial model for investigating viral ion channel function and its effects on host membranes.

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