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      • Record: found
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      Orchestrating mitochondria in neurons: Cytoskeleton as the conductor

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          Abstract

          Mitochondria are crucial to support synaptic activity, particularly through ATP production and Ca 2+ homeostasis. This implies that mitochondria need to be well distributed throughout the different neuronal sub‐compartments. To achieve this, a tight and precise regulation of several neuronal cytoskeleton players is necessary to transport and dock mitochondria. As post‐mitotic cells, neurons are highly dependent on mitochondrial quality control mechanisms and several cytoskeleton proteins have been implicated in mitophagy. Therefore, all of these processes are orchestrated by the crosstalk between mitochondria and the neuronal cytoskeleton to form a coordinated and tuned symphony.

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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 343 times – based on 0 reviews     Review now
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            Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration.

            Zu-Hang Sheng, Qian Cai (2012)
            Mitochondria have a number of essential roles in neuronal function. Their complex mobility patterns within neurons are characterized by frequent changes in direction. Mobile mitochondria can become stationary or pause in regions that have a high metabolic demand and can move again rapidly in response to physiological changes. Defects in mitochondrial transport are implicated in the pathogenesis of several major neurological disorders. Research into the mechanisms that regulate mitochondrial transport is thus an important emerging frontier.
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              Synaptic mitochondria are critical for mobilization of reserve pool vesicles at Drosophila neuromuscular junctions.

              Patrik Verstreken, Cindy V. Ly, Koen J T Venken … (2005)
              In a forward screen for genes affecting neurotransmission in Drosophila, we identified mutations in dynamin-related protein (drp1). DRP1 is required for proper cellular distribution of mitochondria, and in mutant neurons, mitochondria are largely absent from synapses, thus providing a genetic tool to assess the role of mitochondria at synapses. Although resting Ca2+ is elevated at drp1 NMJs, basal synaptic properties are barely affected. However, during intense stimulation, mutants fail to maintain normal neurotransmission. Surprisingly, FM1-43 labeling indicates normal exo- and endocytosis, but a specific inability to mobilize reserve pool vesicles, which is partially rescued by exogenous ATP. Using a variety of drugs, we provide evidence that reserve pool recruitment depends on mitochondrial ATP production downstream of PKA signaling and that mitochondrial ATP limits myosin-propelled mobilization of reserve pool vesicles. Our data suggest a specific role for mitochondria in regulating synaptic strength.
              Article 0 comments Cited 257 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Vanessa Alexandra Morais:
                ORCID: https://orcid.org/0000-0002-0830-0548
                vmorais@medicina.ulisboa.pt
                Journal
                Journal ID (nlm-ta): Cytoskeleton (Hoboken)
                Journal ID (iso-abbrev): Cytoskeleton (Hoboken)
                Journal ID (doi): 10.1002/(ISSN)1949-3592
                Journal ID (publisher-id): CM
                Title: Cytoskeleton (Hoboken, N.j.)
                Publisher: John Wiley & Sons, Inc. (Hoboken, USA )
                ISSN (Print): 1949-3584
                ISSN (Electronic): 1949-3592
                Publication date (Electronic): 09 December 2019
                Publication date (Print): Mar-Apr 2020
                Volume: 77
                Issue: 3-4 , Emerging Concepts of the Neuronal Cytoskeleton ( doiID: 10.1002/cm.v77.3-4 )
                Pages: 65-75
                Affiliations
                [ 1 ] Instituto de Medicina Molecular ‐ João Lobo Antunes, Faculdade de Medicina Universidade de Lisboa Lisbon Portugal
                Author notes
                [*] [* ] Correspondence

                Vanessa Alexandra Morais, Instituto de Medicina Molecular ‐ João Lobo Antunes, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.

                Email: vmorais@ 123456medicina.ulisboa.pt

                Author information
                https://orcid.org/0000-0002-0830-0548
                Article
                Publisher ID: CM21585
                DOI: 10.1002/cm.21585
                PMC ID: 7187307
                PubMed ID: 31782907
                SO-VID: 0e1a2fb3-4d5e-4966-b5ac-7d2438e5bdee
                Copyright © © 2019 The Authors. Cytoskeleton published by Wiley Periodicals, Inc.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 July 2019
                Date revision received : 01 October 2019
                Date accepted : 05 November 2019
                Page count
                Figures: 2, Tables: 0, Pages: 11, Words: 9904
                Funding
                Funded by: FCT ‐ Fundação para a Ciência e Tecnologia
                Award ID: IF/01693/2014
                Award ID: PD/BD/114113/2015
                Award ID: PD/BD/135521/2018
                Award ID: UID/BIM/50005/2019
                Funded by: H2020 European Research Council , open-funder-registry 10.13039/100010663;
                Award ID: ERC‐StG‐679168
                Funded by: European Molecular Biology Organization , open-funder-registry 10.13039/100004410;
                Award ID: EMBO‐IG/3309
                Funded by: European Research Council , open-funder-registry 10.13039/100010663;
                Funded by: Ministério da Ciência, Tecnologia e Ensino Superior , open-funder-registry 10.13039/501100006111;
                Funded by: Fundação para a Ciência e a Tecnologia , open-funder-registry 10.13039/501100001871;
                Categories
                Subject: Minireview
                Subject: Minireviews
                Custom metadata
                source-schema-version-number 2.0
                cover-date March‐April 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.1 mode:remove_FC converted:28.04.2020

                ScienceOpen disciplines: Cell biology
                Keywords: docking,mitochondria,neuronal cytoskeleton,synapse,transport
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: docking, mitochondria, neuronal cytoskeleton, synapse, transport

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