Function and regulation of the divisome for mitochondrial fission
Abstract
Mitochondria form dynamic networks in the cell that are balanced by the flux of iterative fusion and fission events of the organelles. It is now appreciated that mitochondrial fission also represents an end-point event in a signalling axis that allows cells to sense and respond to external cues. The fission process is orchestrated by membrane-associated adaptors, influenced by organellar and cytoskeletal interactions and ultimately executed by the dynamin-like GTPase DRP1. Here we invoke the framework of the 'mitochondrial divisome', which is conceptually and operationally similar to the bacterial cell-division machinery. We review the functional and regulatory aspects of the mitochondrial divisome and, within this framework, parse the core from the accessory machinery. In so doing, we transition from a phenomenological to a mechanistic understanding of the fission process.
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Fragmentation of mitochondrial network facilitates mitophagy, allowing selective clearance of defective mitochondria and preventing excessive ROS production and Ca2+ dyshomeostasis.
“Fragmentation of the mitochondrial network facilitates mitophagy, allowing the selective clearance of defective mitochondria [77] and consequently preventing excessive ROS production and Ca2+ dyshomeostasis.”
From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [77]
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“Notably, newly emerged daughter mitochondria originating from peripheral fi ssion typically lack nucleoids and replicative mitochondrial DNA (mtDNA); instead, they tend to encapsulate damaged constituents and are marked for eventual mitophagic degradation (Kleele et al, 2021; Kraus et al, 2021).”
- Authors
- Kraus, F., Roy, K., Pucadyil, T. J., & Ryan, M. T.
- Affiliations
- Harvard University (US)
- Indian Institute of Science Education and Research Pune (IN)
- Monash University (AU)
- Corresponding author
- Pucadyil, Thomas J.
- Ryan, Michael T.
- Venue
- Nature
- Published
- 2021-02-03
- Volume
- 590
- Issue
- 7844
- Pages
- 57-66
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W3129190575
- Cited by
- 445
- References
- 12
- Citations by year
- 2026: 72 · 2025: 99 · 2024: 113 · 2023: 74 · 2022: 61 · 2021: 26
- FWCI
- 7.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- mitochondrial fission, Drp1, mitochondrial fusion, mitochondrial dynamics, cytoskeletal interactions
- MeSH terms
- Animals, Disease, Biological Evolution, Health, Humans, Mitochondria, Cell Death, Calcium Signaling, Dynamins, Mitochondrial Dynamics
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