Essential factors for maintaining mitochondrial network morphology and cristae shape include OPA1 and MFN2, the dysfunction of which causes an array of phenotypes in D. melanogaster linked to defective mitochondrial architecture, including developmental delay or arrest, cardiomyopathy, and neurological phenotypes resembling autosomal dominant optic atrophy (ADOA) and Charcot–Marie–Tooth type 2A syndrome (CMT2A) [128,129,130,131]. This evidence concerns the gene MFN2 and autosomal dominant optic atrophy.