Mitofusin-2 determines mitochondrial network architecture and mitochondrial metabolism. A novel regulatory mechanism altered in obesity |
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Authors: | Bach Daniel Pich Sara Soriano Francesc X Vega Nathalie Baumgartner Bernhard Oriola Josep Daugaard Jens R Lloberas Jorge Camps Marta Zierath Juleen R Rabasa-Lhoret Rémi Wallberg-Henriksson Harriet Laville Martine Palacín Manuel Vidal Hubert Rivera Francisca Brand Martin Zorzano Antonio |
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Institution: | Parc Cientific de Barcelona, Facultat de Biologia, Universitat de Barcelona, Barcelona 08028, Spain. |
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Abstract: | In many cells and specially in muscle, mitochondria form elongated filaments or a branched reticulum. We show that Mfn2 (mitofusin 2), a mitochondrial membrane protein that participates in mitochondrial fusion in mammalian cells, is induced during myogenesis and contributes to the maintenance and operation of the mitochondrial network. Repression of Mfn2 caused morphological and functional fragmentation of the mitochondrial network into independent clusters. Concomitantly, repression of Mfn2 reduced glucose oxidation, mitochondrial membrane potential, cell respiration, and mitochondrial proton leak. We also show that the Mfn2-dependent mechanism of mitochondrial control is disturbed in obesity by reduced Mfn2 expression. In all, our data indicate that Mfn2 expression is crucial in mitochondrial metabolism through the maintenance of the mitochondrial network architecture, and reduced Mfn2 expression may explain some of the metabolic alterations associated with obesity. |
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