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The myxoma poxvirus protein, M11L, prevents apoptosis by direct interaction with the mitochondrial permeability

Helen Everett1, Michele Barry, Xuejun Sun

  • 1Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G2H7, Canada.

The Journal of Experimental Medicine
|November 6, 2002
PubMed

Insights

Myxoma poxvirus protein M11L binds to the mitochondrial peripheral benzodiazepine receptor (PBR), preventing cell death. This interaction regulates the mitochondrial permeability transition pore, crucial for viral virulence.

Area of Science:

  • Mitochondrial biology
  • Virology
  • Cell death pathways

Background:

  • M11L is an antiapoptotic protein from myxoma poxvirus, essential for virulence.
  • M11L localizes to mitochondria and inhibits apoptosis by preventing mitochondrial membrane potential loss.

Purpose of the Study:

  • To investigate the molecular mechanism by which M11L prevents mitochondrial membrane potential loss.
  • To determine the interaction of M11L with components of the mitochondrial permeability transition (PT) pore.

Main Methods:

  • Cross-linking assays to detect protein-protein interactions.
  • Fluorescence resonance energy transfer (FRET) to confirm M11L and PBR association.
  • Stable and transient expression of M11L in cells.

Main Results:

  • M11L physically associates with the peripheral benzodiazepine receptor (PBR), a component of the PT pore.
  • M11L expression prevents cytochrome c release and mitochondrial membrane potential loss induced by various stimuli.
  • Myxoma virus infection enhances cellular protection from apoptosis in the presence of PBR.

Conclusions:

  • M11L regulates the mitochondrial PT pore complex.
  • M11L likely modulates PBR activity, thereby inhibiting apoptosis.
  • This interaction is critical for myxoma poxvirus virulence.

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