Article
- The EMBO Journal (2009) 28, 1589 - 1600
- doi:10.1038/emboj.2009.89
Published online: 9 April 2009
There is a Have you seen ...? (June 2009) associated with this Article.
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SLP-2 is required for stress-induced mitochondrial hyperfusion
Daniel Tondera1,ab, Stéphanie Grandemange1,ac, Alexis Jourdain1, Mariusz Karbowski2, Yves Mattenberger1, Sébastien Herzig1, Sandrine Da Cruz1,d, Pascaline Clerc3, Ines Raschke4, Carsten Merkwirth4, Sarah Ehses4, Frank Krause5, David C Chan6, Christiane Alexander7, Christoph Bauer8, Richard Youle3, Thomas Langer4 and Jean-Claude Martinou1
- Department of Cell Biology, University of Geneva, Geneva, Switzerland
- Medical Biotechnology Center, University of Maryland Biotechnology Institute, Baltimore, MD, USA
- Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA
- Institute for Genetics and Centre for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany
- Physical Biochemistry, Department of Chemistry, Technische Universität Darmstadt, Darmstadt, Germany
- Division of Biology, California Institute of Technology, Pasadena, CA, USA
- Department of Neuroscience, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany
- Imaging Platform, NCCR Frontiers in Genetics, University of Geneva, Geneva, Switzerland
Correspondence to:
Jean-Claude Martinou, Department of Cell Biology, University of Geneva, 30 quai Ernest-Ansermet, 4 Geneva 1211, Switzerland. Tel.: +41 22 379 6443; Fax: +41 22 379 6442; E-mail: Jean-Claude.Martinou@unige.ch
aThese authors contributed equally to this work
bPresent address: Dana-Farber Cancer Institute, Boston, MA, USA
cPresent address: EA 4001 Predicther, Université Henri Poincaré-Nancy Université, Nancy, France
dPresent address: Ludwig Institute for Cancer Research, University of California San Diego, La Jolla, CA, USA
Received 24 November 2008; Accepted 12 March 2009
Abstract
Mitochondria are dynamic organelles, the morphology of which results from an equilibrium between two opposing processes, fusion and fission. Mitochondrial fusion relies on dynamin-related GTPases, the mitofusins (MFN1 and 2) in the outer mitochondrial membrane and OPA1 (optic atrophy 1) in the inner mitochondrial membrane. Apart from a role in the maintenance of mitochondrial DNA, little is known about the physiological role of mitochondrial fusion. Here we report that mitochondria hyperfuse and form a highly interconnected network in cells exposed to selective stresses. This process precedes mitochondrial fission when it is triggered by apoptotic stimuli such as UV irradiation or actinomycin D. Stress-induced mitochondrial hyperfusion (SIMH) is independent of MFN2, BAX/BAK, and prohibitins, but requires L-OPA1, MFN1, and the mitochondrial inner membrane protein SLP-2. In the absence of SLP-2, L-OPA1 is lost and SIMH is prevented. SIMH is accompanied by increased mitochondrial ATP production and represents a novel adaptive pro-survival response against stress.
Keywords:
- ATP,
- fusion,
- mitochondria,
- stress,
- survival
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