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Updated: Jul 22, 2026

Studying Mitochondrial Structure and Function in Drosophila Ovaries
Published on: January 4, 2017
Breaking the mitochondrial barrier
1Departement de Biologie Cellulaire, Sciences III, 30 quai Ernest Ansermet, 1211 Genève 4, Switzerland. Jean-Claude.Martinou@cellbio.unige.ch.
Abstract:
Pro- and anti-apoptotic members of the Bcl-2 family control the permeability of the outer mitochondrial membrane. They could do this either by forming autonomous pores in the membrane or by collaborating with components of the permeability transition pore. Here we discuss why we favour the first of these possibilities.
Insights
Members of the Bcl-2 family regulate mitochondrial outer membrane permeability. We propose these proteins form pores autonomously, rather than interacting with the permeability transition pore complex.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- The Bcl-2 family comprises key regulators of apoptosis.
- These proteins control the integrity of the outer mitochondrial membrane.
- Their precise mechanism of action remains under investigation.
Purpose of the Study:
- To elucidate the mechanism by which Bcl-2 family proteins regulate mitochondrial outer membrane permeability.
- To evaluate the two proposed models: autonomous pore formation versus interaction with the permeability transition pore complex.
Main Methods:
- Review and critical analysis of existing literature on Bcl-2 family function.
- Biophysical and biochemical data interpretation regarding mitochondrial membrane permeabilization.
Main Results:
- Evidence supports the model where Bcl-2 proteins directly form pores in the outer mitochondrial membrane.
- The alternative model involving collaboration with the permeability transition pore complex is less supported by current data.
Conclusions:
- The Bcl-2 family proteins likely act as autonomous pore-forming units to control mitochondrial outer membrane permeability.
- This mechanism is crucial for the regulation of programmed cell death.
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