The GTPase dMiro is required for axonal transport of mitochondria to drosophila synapses

Xiufang Guo, Greg T. Macleod, Andrea Wellington, Fangle Hu, Sarvari Panchumarthi, Miriam Schoenfield, Leo Marin, Milton P. Charlton, Harold L. Atwood, Konrad E. Zinsmaier

Research output: Contribution to journalArticlepeer-review

411 Scopus citations

Abstract

We have identified EMS-induced mutations in Drosophila Miro (dMiro), an atypical mitochondrial GTPase that is orthologous to human Miro (hMiro). Mutant dmiro animals exhibit defects in locomotion and die prematurely. Mitochondria in dmiro mutant muscles and neurons are abnormally distributed. Instead of being transported into axons and dendrites, mitochondria accumulate in parallel rows in neuronal somata. Mutant neuromuscular junctions (NMJs) lack presynaptic mitochondria, but neurotransmitter release and acute Ca2+ buffering is only impaired during prolonged stimulation. Neuronal, but not muscular, expression of dMiro in dmiro mutants restored viability, transport of mitochondria to NMJs, the structure of synaptic boutons, the organization of presynaptic microtubules, and the size of postsynaptic muscles. In addition, gain of dMiro function causes an abnormal accumulation of mitochondria in distal synaptic boutons of NMJs. Together, our findings suggest that dMiro is required for controlling anterograde transport of mitochondria and their proper distribution within nerve terminals.

Original languageEnglish (US)
Pages (from-to)379-393
Number of pages15
JournalNeuron
Volume47
Issue number3
DOIs
StatePublished - Aug 4 2005

ASJC Scopus subject areas

  • Neuroscience(all)

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