The DOI matches its Crossref record; 63 of the 63 references it cites were found in a registry or an index.
Emerging functions of mammalian mitochondrial fusion and fission
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.
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Cites
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Self-citationDynamin-related Protein Drp1 Is Required for Mitochondrial Division in Mammalian Cells
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The Role of Dynamin-Related Protein 1, a Mediator of Mitochondrial Fission, in Apoptosis
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Mutations in the mitochondrial GTPase mitofusin 2 cause Charcot-Marie-Tooth neuropathy type 2A
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Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376 · cited 1×
“Oxygen electrode studies demonstrate that both endogenous and uncoupled respiration rates are reduced in Mfn-null cells and even more so in cells depleted of OPA1 by RNAi (OPA1–RNAi) (1).”
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Cited by
Mitochondrial membrane permeabilization in cell death
Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Mitochondria: More Than Just a Powerhouse
McBride, H. M., Neuspiel, M., & Wasiak, S. (2006) · Current Biology · doi:10.1016/j.cub.2006.06.054 · Cited by 1,985
Chen, H., Vermulst, M., Wang, Y. E., Chomyn, A., Prolla, T. A., McCaffery, J. M., & Chan, D. C. (2010) · Cell · doi:10.1016/j.cell.2010.02.026 · Cited by 1,211
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The PINK1/Parkin pathway regulates mitochondrial morphology
Poole, A. C., Thomas, R. E., Andrews, L. A., McBride, H. M., Whitworth, A. J., & Pallanck, L. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709336105 · Cited by 885
Metadata
- Authors
- Chen, H., & Chan, D. C.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-10-15
- Volume
- 14
- Issue
- suppl_2
- Pages
- R283-R289
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- OpenAlex
- W2132579877
- Cited by
- 538
- References
- 63
- FWCI
- 10.72
- Type
- journal article
- Language
- en
- Open access
- closed
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