Mutants show loss of anterograde mitochondria transport in motor neurons.
Homozygous olfactory receptor neuron (ORN) clones result in loss of ORN cell bodies and axons. Defects in the organisation of the antennal lobe neuropil, including loss of glomeruli is seen.
Homozygous single cell motor neuron clones in larvae show normal development and axon and synaptic morphology, but show loss of anterograde mitochondria transport.
Wallerian degeneration in an axotomized motor neuron within a crushed, but still continuous segmental nerve follows a similar time course in wild-type and milt33-853 motor neuron clones, with continuity being maintained at 4 hours and a heterogeneous population of continuous and fragmented axons appearing 8 hours after crushing. A significantly smaller fraction of milt33-853 axons are fragmented at 8 hours after crushing compared to wild-type axons, although all mutant and wild-type axons are fragmented by 16 hours after crushing.
milt33-853 has abnormal neuroanatomy | somatic clone | adult stage phenotype, non-suppressible by Scer\GAL4Or22a.7.717/Mmus\WldS.UAS
milt33-853 has adult olfactory receptor neuron | somatic clone phenotype, non-suppressible by Scer\GAL4Or22a.7.717/Mmus\WldS.UAS
milt33-853 has adult antennal lobe | somatic clone phenotype, non-suppressible by Scer\GAL4Or22a.7.717/Mmus\WldS.UAS
milt33-853 has mitochondrion | somatic clone | third instar larval stage phenotype, non-suppressible by Scer\GAL4Toll-6-D42/NmnatUAS.cZa
milt33-853 has motor neuron | somatic clone | third instar larval stage phenotype, non-suppressible by Scer\GAL4Toll-6-D42/NmnatUAS.cZa
The anterograde mitochondria transport defects of single cell milt33-853 larval motor neuron clones are not rescued by expression of NmnatScer\UAS.cZa under the control of Scer\GAL4D42.
Expression of either NmnatScer\UAS.cZa or NmnatWR.Scer\UAS under the control of Scer\GAL4elav-C155 protects both wild-type and milt33-853 motor neuron clones from degeneration after axotomy at 16 hours after crushing.
The loss of olfactory receptor neuron (ORN) cell bodies and axons and the morphological defects in the antennal lobe neuropil which are seen when homozygous milt33-853 ORN clones are induced is not suppressed by expression of Mmus\wldS.Scer\UAS under the control of Scer\GAL4Or22a.7.717.
Expression of Mmus\wldS.Scer\UAS under the control of Scer\GAL4elav-C155 protects both wild-type and milt33-853 motor neuron clones from degeneration after axotomy at 16 hours after crushing and delays Wallerian degeneration in both wild-type and milt33-853 motor neuron clones 24 hours after crushing.