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      Mitochondrial Nanotunnels

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          Abstract

          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.

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          Mitochondrial dynamics--mitochondrial fission and fusion in human diseases.

          Dan L Longo, Stephen Archer (2013)
          Article 0 comments Cited 402 times – based on 0 reviews     Review now
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            A new pathway for mitochondrial quality control: mitochondrial-derived vesicles.

            Ayumu Sugiura, Gian-Luca McLelland, Edward Fon … (2014)
            The last decade has been marked by tremendous progress in our understanding of the cell biology of mitochondria, with the identification of molecules and mechanisms that regulate their fusion, fission, motility, and the architectural transitions within the inner membrane. More importantly, the manipulation of these machineries in tissues has provided links between mitochondrial dynamics and physiology. Indeed, just as the proteins required for fusion and fission were identified, they were quickly linked to both rare and common human diseases. This highlighted the critical importance of this emerging field to medicine, with new hopes of finding drugable targets for numerous pathologies, from neurodegenerative diseases to inflammation and cancer. In the midst of these exciting new discoveries, an unexpected new aspect of mitochondrial cell biology has been uncovered; the generation of small vesicular carriers that transport mitochondrial proteins and lipids to other intracellular organelles. These mitochondrial-derived vesicles (MDVs) were first found to transport a mitochondrial outer membrane protein MAPL to a subpopulation of peroxisomes. However, other MDVs did not target peroxisomes and instead fused with the late endosome, or multivesicular body. The Parkinson's disease-associated proteins Vps35, Parkin, and PINK1 are involved in the biogenesis of a subset of these MDVs, linking this novel trafficking pathway to human disease. In this review, we outline what has been learned about the mechanisms and functional importance of MDV transport and speculate on the greater impact of these pathways in cellular physiology. © 2014 The Authors.
            Article 0 comments Cited 341 times – based on 0 reviews     Review now
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              Transcellular degradation of axonal mitochondria.

              Chung-ha O Davis, Keun-Young Kim, Eric Bushong … (2014)
              It is generally accepted that healthy cells degrade their own mitochondria. Here, we report that retinal ganglion cell axons of WT mice shed mitochondria at the optic nerve head (ONH), and that these mitochondria are internalized and degraded by adjacent astrocytes. EM demonstrates that mitochondria are shed through formation of large protrusions that originate from otherwise healthy axons. A virally introduced tandem fluorophore protein reporter of acidified mitochondria reveals that acidified axonal mitochondria originating from the retinal ganglion cell are associated with lysosomes within columns of astrocytes in the ONH. According to this reporter, a greater proportion of retinal ganglion cell mitochondria are degraded at the ONH than in the ganglion cell soma. Consistently, analyses of degrading DNA reveal extensive mtDNA degradation within the optic nerve astrocytes, some of which comes from retinal ganglion cell axons. Together, these results demonstrate that surprisingly large proportions of retinal ganglion cell axonal mitochondria are normally degraded by the astrocytes of the ONH. This transcellular degradation of mitochondria, or transmitophagy, likely occurs elsewhere in the CNS, because structurally similar accumulations of degrading mitochondria are also found along neurites in superficial layers of the cerebral cortex. Thus, the general assumption that neurons or other cells necessarily degrade their own mitochondria should be reconsidered.
              Article 0 comments Cited 242 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 9200566
                Journal ID (pubmed-jr-id): 21041
                Journal ID (nlm-ta): Trends Cell Biol
                Journal ID (iso-abbrev): Trends Cell Biol.
                Title: Trends in cell biology
                ISSN (Print): 0962-8924
                ISSN (Electronic): 1879-3088
                Publication date Nihms-submitted: 25 September 2017
                Publication date (Electronic): 19 September 2017
                Publication date (Print): November 2017
                Publication date PMC-release: 01 November 2018
                Volume: 27
                Issue: 11
                Pages: 787-799
                Affiliations
                [1 ]Wellcome Trust Centre for Mitochondrial Research, Institute of Neurosciences, Newcastle University, Newcastle upon Tyne, UK
                [2 ]Departamento de Biología Celular y Molecular, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile
                [3 ]MitoCare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA
                [4 ]Division of Behavioral Medicine, Department of Psychiatry, Columbia University Medical Center, New York, NY, USA
                [5 ]Department of Neurology, The Merritt Center and Columbia Translational Neuroscience Initiative, Columbia University Medical Center, New York, NY, USA
                [6 ]Columbia Aging Center, Columbia University Mailman School of Public Health, New York, NY 10032, USA
                Author notes
                [* ] Correspondence: martin.picard@ 123456columbia.edu , (M. Picard)
                Article
                Manuscript ID: NIHMS903147
                DOI: 10.1016/j.tcb.2017.08.009
                PMC ID: 5749270
                PubMed ID: 28935166
                SO-VID: 1d86d0e4-d8d1-4b6d-9d46-eba49f06cf18
                License:

                This is an open access article under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/).

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                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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