SLP-2 is required for stress-induced mitochondrial hyperfusion.

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Serval ID
serval:BIB_FD68C8D3A934
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
SLP-2 is required for stress-induced mitochondrial hyperfusion.
Journal
The EMBO journal
Author(s)
Jourdain Alexis
Publication state
Published
Issued date
09/04/2009
Language
english
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.
Pubmed
Create date
13/04/2021 17:25
Last modification date
14/04/2021 6:37
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