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1. Nitric oxide inhibition of Drp1-mediated mitochondrial fission is critical for myogenic differentiation.

Author

De Palma C, Falcone S, Pisoni S, Cipolat S, Panzeri C, Pambianco S, Pisconti A, Allevi R, Bassi MT, Cossu G, Pozzan T, Moncada S, Scorrano L, Brunelli S, and Clementi E

Subjects
Animals, Apoptosis, Cell Respiration, Cyclic GMP metabolism, Dynamins, Guanylate Cyclase metabolism, Immunoblotting, Mice, Microscopy, Confocal, Microscopy, Electron, Transmission, Mitochondria, Muscle physiology, Mitochondria, Muscle ultrastructure, Mitochondrial Proteins metabolism, Myoblasts metabolism, Myoblasts ultrastructure, Nitric Oxide biosynthesis, Cell Differentiation, GTP Phosphohydrolases metabolism, Microtubule-Associated Proteins metabolism, Mitochondria, Muscle metabolism, Muscle Development physiology, Myoblasts cytology, Nitric Oxide metabolism
Abstract

During myogenic differentiation the short mitochondria of myoblasts change into the extensively elongated network observed in myotubes. The functional relevance and the molecular mechanisms driving the formation of this mitochondrial network are unknown. We now show that mitochondrial elongation is required for myogenesis to occur and that this event depends on the cellular generation of nitric oxide (NO). Inhibition of NO synthesis in myogenic precursor cells leads to inhibition of mitochondrial elongation and of myogenic differentiation. This is due to the enhanced activity, translocation and docking of the pro-fission GTPase dynamin-related protein-1 (Drp1) to mitochondria, leading also to a latent mitochondrial dysfunction that increased sensitivity to apoptotic stimuli. These effects of NO inhibition were not observed in myogenic precursor cells containing a dominant-negative form of Drp1. Both NO-dependent repression of Drp1 action and maintenance of mitochondrial integrity and function were mediated through the soluble guanylate cyclase. These data uncover a novel level of regulation of differentiation linking mitochondrial morphology and function to myogenic differentiation.

Published
2010
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2. Nitric oxide inhibition of Drp1-mediated mitochondrial fission is critical for myogenic differentiation

Author

Sara Cipolat, C. De Palma, Emilio Clementi, S. Pisoni, Giulio Cossu, Silvia Brunelli, Sarah Pambianco, Chris Panzeri, Sestina Falcone, Salvador Moncada, Tullio Pozzan, Addolorata Pisconti, Raffaele Allevi, Maria Teresa Bassi, Luca Scorrano, De Palma, C, Falcone, S, Pisoni, S, Cipolat, S, Panzeri, C, Pambianco, S, Pisconti, A, Allevi, R, Bassi, M, Cossu, G, Pozzan, T, Moncada, S, Scorrano, L, Brunelli, S, and Clementi, E

Subjects
Mitochondria, Muscle/*metabolism/physiology/ultrastructure, Cellular differentiation, Apoptosis, Mitochondrion, Muscle Development, GTP Phosphohydrolases, GTP Phosphohydrolase, Myoblasts, chemistry.chemical_compound, Mice, 0302 clinical medicine, Myocyte, Cyclic GMP, 0303 health sciences, Microscopy, Confocal, ATP synthase, Myogenesis, Cell Differentiation, Cell biology, Mitochondrial fission, Signal transduction, Myoblasts/*cytology/metabolism/ultrastructure, Guanylate Cyclase/metabolism, Microtubule-Associated Proteins, Nitric Oxide/biosynthesis/*metabolism, Dynamins, Myoblast, Mitochondrial Proteins/metabolism, Cell Respiration, Immunoblotting, Microtubule-Associated Proteins/*metabolism, Biology, Nitric Oxide, Article, Nitric oxide, Mitochondrial Proteins, 03 medical and health sciences, Microscopy, Electron, Transmission, Mitochondrial Protein, Animals, ddc:612, Molecular Biology, 030304 developmental biology, Muscle Development/*physiology, Animal, Microtubule-Associated Protein, Apoptosi, Cell Biology, Mitochondria, Muscle, Cyclic GMP/metabolism, chemistry, Guanylate Cyclase, biology.protein, GTP Phosphohydrolases/*metabolism, 030217 neurology & neurosurgery
Abstract

During myogenic differentiation the short mitochondria of myoblasts change into the extensively elongated network observed in myotubes. The functional relevance and the molecular mechanisms driving the formation of this mitochondrial network are unknown. We now show that mitochondrial elongation is required for myogenesis to occur and that this event depends on the cellular generation of nitric oxide (NO). Inhibition of NO synthesis in myogenic precursor cells leads to inhibition of mitochondrial elongation and of myogenic differentiation. This is due to the enhanced activity, translocation and docking of the pro-fission GTPase dynamin-related protein-1 (Drp1) to mitochondria, leading also to a latent mitochondrial dysfunction that increased sensitivity to apoptotic stimuli. These effects of NO inhibition were not observed in myogenic precursor cells containing a dominant-negative form of Drp1. Both NO-dependent repression of Drp1 action and maintenance of mitochondrial integrity and function were mediated through the soluble guanylate cyclase. These data uncover a novel level of regulation of differentiation linking mitochondrial morphology and function to myogenic differentiation. © 2010 Macmillan Publishers Limited All rights reserved.

Published
2010

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