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Emerging functions of mammalian mitochondrial fusion and fission

Chen, Hsiuchen and Chan, David C. (2005) Emerging functions of mammalian mitochondrial fusion and fission. Human Molecular Genetics, 14 (2). R283-R289. ISSN 0964-6906. http://resolver.caltech.edu/CaltechAUTHORS:CHEhmg05

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Abstract

Mitochondria provide a myriad of services to the cell, including energy production, calcium buffering and regulation of apoptosis. How these diverse functions are coordinated among the hundreds of mitochondria in a given cell is largely unknown, but is probably dependent on the dynamic nature of mitochondria. In this review, we explore the latest developments in mitochondrial dynamics in mammals. These studies indicate that mitofusins and OPA1 are essential for mitochondrial fusion, whereas Fis1 and Drp1 are essential for mitochondrial fission. The overall morphology of the mitochondrial population depends on the relative activities of these two sets of proteins. In addition to the regulation of mitochondrial shape, these molecules also play important roles in cell and tissue physiology. Perturbation of mitochondrial fusion results in defects in mitochondrial membrane potential and respiration, poor cell growth and increased susceptibility to cell death. These cellular observations may explain why mitochondrial fusion is essential for embryonic development. Two inherited neuropathies, Charcot–Marie–Tooth type 2A and autosomal dominant optic atrophy, are caused by mutations in mitofusin 2 and OPA1, suggesting that proper regulation of mitochondrial dynamics is particularly vital to neurons. Mitochondrial fission accompanies several types of apoptotic cell death and appears important for progression of the apoptotic pathway. These studies provide insight into how mitochondria communicate with one another to coordinate mitochondrial function and morphology.


Item Type:Article
Additional Information:© The Author 2005. Published by Oxford University Press. Received June 8, 2005; accepted July 14, 2005. Conflict of Interest statement. None declared.
Subject Keywords:DOMINANT OPTIC ATROPHY; DYNAMIN-RELATED PROTEIN; MARIE-TOOTH-DISEASE; WD REPEAT PROTEIN; OPA1 MUTATIONS; APOPTOSIS; GTPASE; MORPHOLOGY; DIVISION; CELLS
Record Number:CaltechAUTHORS:CHEhmg05
Persistent URL:http://resolver.caltech.edu/CaltechAUTHORS:CHEhmg05
Alternative URL:http://dx.doi.org/doi:10.1093/hmg/ddi270
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:5765
Collection:CaltechAUTHORS
Deposited By: Lindsay Cleary
Deposited On:01 Nov 2006
Last Modified:26 Dec 2012 09:15

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