期刊
EMBO JOURNAL
卷 28, 期 11, 页码 1589-1600出版社
WILEY
DOI: 10.1038/emboj.2009.89
关键词
ATP; fusion; mitochondria; stress; survival
资金
- Deutsche Forschungsgemeinschaft (DFG) [TO540/1-1]
- NIH
- Swiss National Science Foundation [3100A0-109419/1]
- Oncosuisse Trust
- Roche Reasearch Foundation
- Geneva Department of Education
- European Union [LSHM-CT-2004-512020]
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. The EMBO Journal (2009) 28, 1589-1600. doi:10.1038/emboj.2009.89; Published online 9 April 2009
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