Mfn1 is an outer-mitochondrial-membrane mitofusin that promotes mitochondrial fusion through a GTP-dependent mechanism. It forms complexes with itself and with Mfn2. Fusion lets separate mitochondria exchange components, contributing to maintenance of a functional mitochondrial network. [ref]
Mouse fibroblasts deficient in Mfn1 showed a severe reduction in fusion and fragmented organelles. Rescue experiments supported a causal role for Mfn1, while comparison with Mfn2-deficient cells revealed overlapping and distinct functions. The combination of genetic loss, direct fusion assessment and rescue is more informative than inferring a fusion mechanism from a still image of mitochondrial shape.
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