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Published on: April 21, 2015
Influenza virus M2 integral membrane protein is a homotetramer stabilized by formation of disulfide bonds
1Department of Biochemistry, Molecular and Cell Biology, Northwestern University, Evanston, Illinois 60208-3500.
Abstract:
The oligomeric structure of the influenza A virus M2 integral membrane protein was determined. On SDS-polyacrylamide gels under nonreducing conditions, the influenza A/Udorn/72 virus M2 forms disulfide-linked dimers (30 kDa) and tetramers (60 kDa). Sucrose gradient analysis and chemical cross-linking analysis indicated that the oligomeric form of M2 is a tetramer consisting of either a pair of disulfide-linked dimers or disulfide-linked tetramers. In addition, a small amount of a cross-linked species of 150-180,000 kDa, which the available data suggest contains only M2 polypeptides, was observed. The role of M2 cysteine residues in disulfide bond formation and their role in forming oligomers were examined by converting each of the two extracellular and single cytoplasmic cysteine residues to serine residues and expressing the altered M2 proteins in eukaryotic cells. Removal of either one of the N-terminal cysteines at residues 17 or 19 indicated that tetramers formed that consisted of a pair of noncovalently associated disulfide-linked dimers, suggesting that each of the cysteine residues is equally competent for forming disulfide bonds. When both cysteine residues were removed from the M2 N-terminal domain, no disulfide-linked forms were observed. When solubilized in detergent this double-cysteine mutant lost reactivity with a M2-specific mAb and exhibited an altered sedimentation pattern on sucrose gradients. However, chemical cross-linking of this double-cysteine mutant in membranes indicated that it can form tetramers. Taken together, these data suggest that disulfide bond formation, although not essential for oligomeric assembly, stabilizes the M2 tetramer from disruption by detergent solubilization.
Insights
The influenza A virus M2 protein forms stable tetramers, with disulfide bonds crucial for stabilizing this structure against detergent disruption. These bonds are formed by N-terminal cysteine residues, essential for M2 protein function.
Area of Science:
- Biochemistry
- Virology
- Structural Biology
Background:
- The M2 protein is an integral membrane protein of the influenza A virus.
- Understanding the M2 protein's oligomeric structure is key to its function and potential drug targeting.
Purpose of the Study:
- To determine the oligomeric structure of the influenza A virus M2 protein.
- To investigate the role of M2 cysteine residues in disulfide bond formation and oligomer assembly.
Main Methods:
- SDS-polyacrylamide gel electrophoresis (non-reducing conditions)
- Sucrose gradient analysis
- Chemical cross-linking analysis
- Site-directed mutagenesis of M2 cysteine residues
- Expression in eukaryotic cells
Main Results:
- Influenza A virus M2 protein forms disulfide-linked dimers and tetramers.
- The M2 oligomer is predominantly a tetramer, stabilized by disulfide bonds involving N-terminal cysteine residues.
- Disulfide bond formation is not essential for tetramer assembly but stabilizes the structure against detergent solubilization.
Conclusions:
- Disulfide bonds play a critical role in stabilizing the M2 tetramer.
- The N-terminal cysteine residues are competent for forming disulfide bonds, contributing to M2 protein stability.
- The M2 tetramer's stability is important for its function and integrity.
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