A 29 bp deletion and frame-shifts Miro at Y89, adding 12 abnormal amino acids before terminating.
Homozygous ventral midline precursor cells do not divide more often than wild-type precursors.
Heterozygous MiroSd32 mutants display mitochondrial mislocalisation in neurons.
In the motor neurons of MiroB682/MiroSd32 larvae, mitochondria are largely absent from neuro-muscular junctions, and are present in reduced numbers in axons, mainly concentrated close to the ventral ganglion. The proportion of motile mitochondria is significantly reduced in these cells and, unlike in wild-type, many stationary mitochondria are not clustered. In addition, the motile mitochondria (both anterograde and retrograde) are significantly smaller than in wild-type.
Gross eye morphology is normal but phototaxis is defective in flies whose eyes are homozygous for MiroSd32.
In neurons of MiroSd32/MiroB682 larvae, mitochondria are retained in the cell bodies and not properly distributed to neuronal processes - most neuromuscular junctions lack mitochondria.
Bouton morphology and distribution is abnormal at neuromuscular junctions in MiroB682/MiroSd32 larvae.
In MiroSd32/MiroB682 larvae, excitatory junction potential evoked by 10Hz stimulation of neuro-muscular junctions (NMJs) starts off normal, but, unlike wild-type, rapidly decays.
MiroSd32/Miro[+] is an enhancer of abnormal locomotor behavior phenotype of Hsap\APPAβ42.UAS.Tag:SS(rPENK), Scer\GAL4elav-C155
MiroSd32 is a non-suppressor of eye photoreceptor cell | somatic clone phenotype of SdhA1110
MiroSd32 heterozygosity enhances the locomotor defects in flies induced by Scer\GAL4elav-C155-driven overexpression of Hsap\APPAβ1-42.Scer\UAS.cIa.
MiroSd32/MiroB682 is partially rescued by Scer\GAL4RapGAP1-OK6/MiroUAS.Tag:MYC