| First Author | Tondera D | Year | 2009 |
| Journal | EMBO J | Volume | 28 |
| Issue | 11 | Pages | 1589-600 |
| PubMed ID | 19360003 | Mgi Jnum | J:149906 |
| Mgi Id | MGI:3849358 | Doi | 10.1038/emboj.2009.89 |
| Citation | Tondera D, et al. (2009) SLP-2 is required for stress-induced mitochondrial hyperfusion. EMBO J 28(11):1589-600 |
| abstractText | 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. |
