The mitochondria are dynamic organelles that constantly fuse and divide. An 
equilibrium between fusion and fission controls the morphology of the 
mitochondria, which appear as dots or elongated tubules depending the prevailing 
force. Characterization of the components of the fission and fusion machineries 
has progressed considerably, and the emerging question now is what role 
mitochondrial dynamics play in mitochondrial and cellular functions. Its 
importance has been highlighted by the discovery that two human diseases are 
caused by mutations in the two mitochondrial pro-fusion genes, MFN2 and OPA1. 
This review will focus on data concerning the function of OPA1, mutations in 
which cause optic atrophy, with respect to the underlying pathophysiological 
processes.