Required for mitochondrial complex IV activity. May be involved in non-associative learning. RNAi-mediated knockdown of the protein causes complete lethality at a late pupal stage. Muscle-specific knockdown is lethal under strongly induced conditions, but shows no obvious alteration in locomotion and behavior under mild induction conditions. Neuron-specific knockdown flies show striking motor defects. Analysis of synaptic and subsynaptic organization at larval neuromuscular junction shows normal overall synapse morphology, but a highly significant decrease in the amount of active zones, i.e. presynaptic microdomains of neurotransmitter release. Muscle size is smaller in knockdown animals compared to wild-type. Neuron-specific knockdown flies show decreased ability for non-associative learning, tested by non-associative jump-reflex habituation. Wing-specific knockdown produces flies with a dramatically reduced wing size. Eye-specific knockdown disturbs ommatidia and bristle organization and corrupts integrity of mitochondria. Electroretinograms show a gross defect in basal neurotransmission.