Journal
ELIFE
Volume 3, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.03558
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Funding
- Intellectual and Developmental Disabilities Research Center [NIH 5P30HD024064]
- NIH [5R01GM067858, T32 NS043124-11, 5T32HD055200, RC4GM096355-01]
- Research Education and Career Horizon Institutional Research and Academic Career Development Award Fellowship [5K12GM084897]
- Edward and Josephine Hudson Scholarship Fund
- Houston Laboratory and Population Science Training Program in Gene-Environment Interaction from the Burroughs Wellcome Fund [1008200]
- National Science Council [NSC-095-SAF-I-564-015-TMS]
- Nakajima Foundation
- Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital
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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.
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