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SLP-2 is required for stress-induced mitochondrial hyperfusion

Item Type:Article
Title:SLP-2 is required for stress-induced mitochondrial hyperfusion
Creators Name:Tondera, D. and Grandemange, S. and Jourdain, A. and Karbowski, M. and Mattenberger, Y. and Herzig, S. and Da Cruz, S. and Clerc, P. and Raschke, I. and Merkwirth, C. and Ehses, S. and Krause, F. and Chan, D.C. and Alexander, C. and Bauer, C. and Youle, R. and Langer, T. and Martinou, J.C.
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, Animals, Mice
Source:EMBO Journal
Publisher:Nature Publishing Group
Page Range:1589-1600
Date:3 June 2009
Official Publication:https://doi.org/10.1038/emboj.2009.89
PubMed:View item in PubMed

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