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    Zc3h10 is a novel mitochondrial regulator

    265650.pdf (2.089Mb)
    Access Status
    Open access
    Authors
    Audano, M.
    Pedretti, S.
    Cermenati, G.
    Brioschi, E.
    Diaferia, G.
    Ghisletti, S.
    Cuomo, A.
    Bonaldi, T.
    Salerno, F.
    Mora, M.
    Grigore, L.
    Garlaschelli, K.
    Baragetti, A.
    Bonacina, F.
    Catapano, A.
    Norata, Giuseppe
    Crestani, M.
    Caruso, D.
    Saez, E.
    De Fabiani, E.
    Mitro, N.
    Date
    2018
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Audano, M. and Pedretti, S. and Cermenati, G. and Brioschi, E. and Diaferia, G. and Ghisletti, S. and Cuomo, A. et al. 2018. Zc3h10 is a novel mitochondrial regulator. EMBO Reports. 19 (4): Article ID e45531.
    Source Title
    EMBO Reports
    DOI
    10.15252/embr.201745531
    ISSN
    1469-221X
    School
    School of Pharmacy and Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/66790
    Collection
    • Curtin Research Publications
    Abstract

    Mitochondria are the energy-generating hubs of the cell. In spite of considerable advances, our understanding of the factors that regulate the molecular circuits that govern mitochondrial function remains incomplete. Using a genome-wide functional screen, we identify the poorly characterized protein Zinc finger CCCH-type containing 10 (Zc3h10) as regulator of mitochondrial physiology. We show that Zc3h10 is upregulated during physiological mitochondriogenesis as it occurs during the differentiation of myoblasts into myotubes. Zc3h10 overexpression boosts mitochondrial function and promotes myoblast differentiation, while the depletion of Zc3h10 results in impaired myoblast differentiation, mitochondrial dysfunction, reduced expression of electron transport chain (ETC) subunits, and blunted TCA cycle flux. Notably, we have identified a loss-of-function mutation of Zc3h10 in humans (Tyr105 to Cys105) that is associated with increased body mass index, fat mass, fasting glucose, and triglycerides. Isolated peripheral blood mononuclear cells from individuals homozygotic for Cys105 display reduced oxygen consumption rate, diminished expression of some ETC subunits, and decreased levels of some TCA cycle metabolites, which all together derive in mitochondrial dysfunction. Taken together, our study identifies Zc3h10 as a novel mitochondrial regulator.

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