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Lookup NU author(s): Dr Amy VincentORCiD, Emeritus Professor Doug Turnbull
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2017 The Authors. Insight into the regulation of complex physiological systems emerges from understanding how biological units communicate with each other. Recent findings show that mitochondria communicate at a distance with each other via nanotunnels, thin double-membrane protrusions that connect the matrices of non-adjacent mitochondria. Emerging evidence suggest that mitochondrial nanotunnels are generated by immobilized mitochondria and transport proteins. This review integrates data from the evolutionarily conserved structure and function of intercellular projections in bacteria with recent developments in mitochondrial imaging that permit nanotunnel visualization in eukaryotes. Cell type-specificity, timescales, and the selective size-based diffusion of biomolecules along nanotunnels are also discussed. The joining of individual mitochondria into dynamic networks of communicating organelles via nanotunnels and other mechanisms has major implications for organelle and cellular behaviors. Nanotunnels are communicating double-membrane tubular protrusions 40-200. nm in diameter, and up to 30. μm in length, that emerge primarily from the surface of immobilized mitochondria or from mitochondria in tissues with restricted mitochondrial motility.Nanotunnels transport matrix and membrane proteins between mitochondria, and probably also transport smaller molecules such as ions, RNA, and metabolites.In a cell-free system, microtubules, mitochondria, ATP, and kinesin 5b are sufficient to produce mitochondrial protrusions, whereas disruption of microtubules hinders nanotunnel formation, implicating a motor-driven microtubule-dependent mechanism of nanotunnel formation.Disruption of calcium dynamics in muscle cells and genetic mitochondrial defects are associated with greater abundance of mitochondrial nanotunnels, suggesting that nanotunnels arise as a compensatory mechanism to promote mitochondrial communication in stress conditions.
Author(s): Vincent AE, Turnbull DM, Eisner V, Hajnóczky G, Picard M
Publication type: Article
Publication status: Published
Journal: Trends in Cell Biology
Year: 2017
Volume: 27
Issue: 11
Pages: 787-799
Print publication date: 01/11/2017
Online publication date: 19/09/2017
Acceptance date: 02/04/2016
Date deposited: 09/11/2017
ISSN (print): 0962-8924
ISSN (electronic): 1879-3088
Publisher: Elsevier Ltd
URL: https://doi.org/10.1016/j.tcb.2017.08.009
DOI: 10.1016/j.tcb.2017.08.009
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