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SLP‐2 is required for stress‐induced mitochondrial hyperfusion
Author(s) -
Tondera Daniel,
Grandemange Stéphanie,
Jourdain Alexis,
Karbowski Mariusz,
Mattenberger Yves,
Herzig Sébastien,
Da Cruz Sandrine,
Clerc Pascaline,
Raschke Ines,
Merkwirth Carsten,
Ehses Sarah,
Krause Frank,
Chan David C,
Alexander Christiane,
Bauer Christoph,
Youle Richard,
Langer Thomas,
Martinou JeanClaude
Publication year - 2009
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2009.89
Subject(s) - mfn1 , mfn2 , mitochondrial fusion , mitochondrial fission , biology , microbiology and biotechnology , mitochondrial carrier , mitochondrion , dnaja3 , mitochondrial apoptosis induced channel , atp–adp translocase , translocase of the inner membrane , inner mitochondrial membrane , mitochondrial dna , translocase of the outer membrane , dynamin , hsp60 , bacterial outer membrane , mitochondrial membrane transport protein , heat shock protein , genetics , cell , hsp70 , endocytosis , gene , escherichia coli
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.