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Mitochondrial fusion and fission affect the distribution and quality control of mitochondria. We show that Marf (Mitochondrial associated regulatory factor), is required for mitochondrial fusion and transport in long axons. Moreover, loss of  Marf  leads to a severe depletion of mitochondria in neuromuscular junctions (NMJs).  Marf  mutants also fail to maintain proper synaptic transmission at NMJs upon repetitive stimulation, similar to  Drp1  fission mutants. However, unlike  Drp1 , loss of  Marf  leads to NMJ morphology defects and extended larval lifespan. Marf is required to form contacts between the endoplasmic reticulum and/or lipid droplets (LDs) and for proper storage of cholesterol and ecdysone synthesis in ring glands. Interestingly, human Mitofusin-2 rescues the loss of LD but both Mitofusin-1 and Mitofusin-2 are required for steroid-hormone synthesis. Our data show that Marf and Mitofusins share an evolutionarily conserved role in mitochondrial transport, cholesterol ester storage and steroid-hormone synthesis.

Mitochondrial fusion but not fission regulates larval growth and synaptic development through steroid hormone production