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Scientific article
Open access
English

SLP-2 is required for stress-induced mitochondrial hyperfusion

Published inEMBO journal, vol. 28, no. 11, p. 1589-1600
Publication date2009
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
  • Adenosine Triphosphate/metabolism
  • Animals
  • Cells, Cultured
  • Dactinomycin/toxicity
  • Fibroblasts/drug effects/physiology/radiation effects
  • GTP Phosphohydrolases/physiology
  • Membrane Proteins/physiology
  • Mice
  • Mitochondria/drug effects/metabolism/physiology/radiation effects
  • Stress, Physiological
  • Ultraviolet Rays
Citation (ISO format)
TONDERA, Daniel et al. SLP-2 is required for stress-induced mitochondrial hyperfusion. In: EMBO journal, 2009, vol. 28, n° 11, p. 1589–1600. doi: 10.1038/emboj.2009.89
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Article (Published version)
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ISSN of the journal0261-4189
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