Mitochondrial outer membrane GTPase that mediates mitochondrial clustering and fusion (PubMed:12527753, PubMed:23921378, PubMed:23620051). Mitochondria are highly dynamic organelles, and their morphology is determined by the equilibrium between mitochondrial fusion and fission events. Overexpression induces the formation of mitochondrial networks. Membrane clustering requires GTPase activity and may involve a major rearrangement of the coiled coil domains (By similarity). Plays a central role in mitochondrial metabolism and may be associated with obesity and/or apoptosis processes. Plays an important role in the regulation of vascular smooth muscle cell proliferation (By similarity). Involved in the clearance of damaged mitochondria via selective autophagy (mitophagy). Is required for PRKN recruitment to dysfunctional mitochondria (PubMed:23620051). Involved in the control of unfolded protein response (UPR) upon ER stress including activation of apoptosis and autophagy during ER stress (PubMed:23921556). Acts as an upstream regulator of EIF2AK3 and suppresses EIF2AK3 activation under basal conditions (PubMed:23921556). GTP + H2O = GDP + H(+) + phosphate Forms homomultimers and heteromultimers with MFN1 (PubMed:12527753). Oligomerization is essential for mitochondrion fusion (Probable). Interacts with VAT1 (By similarity). Interacts with STOML2; may form heterooligomers (By similarity). Interacts (phosphorylated) with PRKN (PubMed:23620051). Interacts with EIF2AK3 (By similarity). Interacts with THG1L; THG1L probably functions as a guanyl-nucleotide exchange factor/GEF, activating MFN2. Colocalizes with BAX during apoptosis. Ubiquitous. Expression is markedly reduced in ApoE-knockout mouse atherosclerotic arteries. A helix bundle is formed by helices from the N-terminal and the C-terminal part of the protein. The GTPase domain cannot be expressed by itself, without the helix bundle. Rearrangement of the helix bundle and/or of the coiled coil domains may bring membranes from adjacent mitochondria into close contact, and thereby play a role in mitochondrial fusion. Phosphorylated by PINK1. Ubiquitinated by non-degradative ubiquitin by PRKN, promoting mitochondrial fusion; deubiquitination by USP30 inhibits mitochondrial fusion (PubMed:23620051, PubMed:24513856). Ubiquitinated by HUWE1 when dietary stearate (C18:0) levels are low; ubiquitination inhibits mitochondrial fusion (By similarity). Mutant mice die early during embryonic development (PubMed:12527753). Heart-specific disruption causes cardiomyopathy in aging mice, characterized by dilated hearts that are insensitive to beta-adrenergic stimulation and impaired contractile performance (PubMed:23620051). Mutant cardiomyocytes display mitochondrial enlargement with respiratory impairment (PubMed:23620051). Belongs to the TRAFAC class dynamin-like GTPase superfamily. Dynamin/Fzo/YdjA family. Mitofusin subfamily. Extended N-terminus.