SLP-2 is required for stress-induced mitochondrial hyperfusion

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Item Type:	Article
Title:	SLP-2 is required for stress-induced mitochondrial hyperfusion
Creators Name:	Tondera, D., Grandemange, S., Jourdain, A., Karbowski, M., Mattenberger, Y., Herzig, S., Da Cruz, S., Clerc, P., Raschke, I., Merkwirth, C., Ehses, S., Krause, F., Chan, D.C., Alexander, C., Bauer, C., Youle, R., 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
ISSN:	0261-4189
Publisher:	Nature Publishing Group
Volume:	28
Number:	11
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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