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Journal Article
Functions and dysfunctions of mitochondrial dynamics
2007
Overview
Key Points
Mitochondria are dynamic organelles. They continually fuse and divide, are actively recruited to specific cellular locations and have dynamic structures.
Mitochondrial fusion requires three large GTPases: the outer membrane proteins MFN1 and MFN2, and the inner membrane protein OPA1.
Mitochondrial fission requires the dynamin GTPase DRP1 and the outer membrane protein FIS1.
The fusion and fission of mitochondria have several important functions. These processes control the morphology of mitochondria, allow content exchange between mitochondria, control mitochondrial distribution and facilitate the release of intermembrane space proteins during apoptosis.
Several structural changes in mitochondria are important for rapid and efficient apoptosis: the mitochondria must be fragmented, their outer membranes must become permeable and the cristae junctions must be widened.
Mitochondrial dynamics is particularly important to neurons, and defects result in neurodegenerative disease.
Mitochondria constantly fuse and divide, are actively transported to specific subcellular localizations and have dynamic structures. Mitochondrial dynamics is important for the functional state of mitochondria, and defects can manifest in mammalian development, apoptosis and neurodegenerative disease.
Recent findings have sparked renewed appreciation for the remarkably dynamic nature of mitochondria. These organelles constantly fuse and divide, and are actively transported to specific subcellular locations. These dynamic processes are essential for mammalian development, and defects lead to neurodegenerative disease. But what are the molecular mechanisms that control mitochondrial dynamics, and why are they important for mitochondrial function? We review these issues and explore how defects in mitochondrial dynamics might cause neuronal disease.
Publisher
Nature Publishing Group UK,Nature Publishing Group
