A trial of mitofusin activation shows neuron regeneration and phenotype reversal in vitro and in vivo in experimental Charcot–Marie–Tooth disease type 2A caused by mitofusin 2 mutations.

A combination of an in vitro mitochondrial fusion assay with electron cryo-tomography (cryo-ET) reveals distinct steps and protein complexes during mitofusin-dependent fusion between adjacent mitochondrial outer membranes.

A potential medication has been found for the brain and muscle degenerative diseases caused by mutant forms of Valosin-Containing Protein.

By reducing mitochondrial fusion, MUL1 compensates for the mutations in PINK1 or parkin that underlie certain cases of Parkinson's disease.

Specific human mitofusin 2 mutations induce selective upper body obesity with suppressed leptin expression and severe adipose mitochondrial dysfunction.

A signaling pathway—comprising a linear sequence of the ubiquitin-selective chaperone Cdc48/p97 and the deubiquitylases Ubp12 and Ubp2—synergistically regulates mitochondrial fusion, thereby fine-tuning ubiquitylation of the mitofusin Fzo1.

Mitochondrial fusion enables a metabolic transition during spermatogenesis.

The dual role of Drosophila Mitofusin in steroid hormone production and cholesterol ester storage, which is evolutionary conserved by the combined expression of the two mammalian Mitofusins, ensures proper synaptic development.

Interactions between Aim24 and the mitochondrial outer and inner membrane contact site complex (MICOS) are essential for mitochondrial ultrastructure, lipid composition and oxidative phosphorylation.

Genetic and electrophysiological experiments reveal that a gene called MCU encodes the ion channel pore that allows calcium ions to cross the inner mitochondrial membrane.