Dynamin-related GTPase that is essential for normal mitochondrial morphology by regulating the equilibrium between mitochondrial fusion and mitochondrial fission (PubMed:11847212, PubMed:24616225, PubMed:26785494, PubMed:28746876). Coexpression of isoform 1 with shorter alternative products is required for optimal activity in promoting mitochondrial fusion (By similarity). Binds lipid membranes enriched in negatively charged phospholipids, such as cardiolipin, and promotes membrane tubulation. The intrinsic GTPase activity is low, and is strongly increased by interaction with lipid membranes (By similarity). Plays a role in remodeling cristae and the release of cytochrome c during apoptosis (PubMed:16839884, PubMed:16839885). Proteolytic processing in response to intrinsic apoptotic signals may lead to disassembly of OPA1 oligomers and release of the caspase activator cytochrome C (CYCS) into the mitochondrial intermembrane space (PubMed:16839884, PubMed:16839885). Plays a role in mitochondrial genome maintenance (By similarity). Produced by cleavage at position S1 by OMA1 following stress conditions that induce loss of mitochondrial membrane potential, leading to negative regulation of mitochondrial fusion. Isoforms that contain the alternative exon 4b (present in isoform 2, but not in isoform 1) are required for mitochondrial genome maintenance, possibly by anchoring the mitochondrial nucleoids to the inner mitochondrial membrane. GTP + H2O = GDP + H(+) + phosphate Activated by guanine nucleotide exchange factor RCC1L. Oligomeric complex consisting of membrane-bound and soluble forms of OPA1 (PubMed:16839885). Interacts with CHCHD3 and IMMT; these interactions occur preferentially with soluble OPA1 forms (PubMed:21081504). Interacts with RCC1L; this interaction is direct (PubMed:28746876). Binds PARL (PubMed:16839884). Interacts with PRELID1 (By similarity). Detected at contact sites between endoplasmic reticulum and mitochondrion membranes. Detected in brain (at protein level) (PubMed:11847212). Detected in brain, brain stem, heart, kidney, liver and skeletal muscle (PubMed:11847212). PARL-dependent proteolytic processing releases an antiapoptotic soluble form not required for mitochondrial fusion (PubMed:20038678, PubMed:24550258, PubMed:22433842). Cleaved by OMA1 at position S1 following stress conditions (PubMed:20038678, PubMed:24550258, PubMed:22433842). Cleavage at position S2 is mediated by YME1L (PubMed:24616225, PubMed:26785494). Cleavage may occur in the sequence motif Leu-Gln-Gln-Gln-Ile-Gln (LQQQIQ) (By similarity). Embryonic fibroblasts that lack Opa1 show a defect in apoptosis in response to intrinsic signals. This defect can be complemented by a soluble form of Opa1 targeted to the mitochondrial intermembrane space. Belongs to the TRAFAC class dynamin-like GTPase superfamily. Dynamin/Fzo/YdjA family.