|Feature type||allele||Associated gene||Dmel\Manf|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
neurite & dopaminergic neuron | larval stage
Homozygotes die as later first instar larvae or immediately after the delayed first moult with defects in behaviour; the larvae atypically wander away from the food, then move more slowly and finally freeze, immobilised but still responding to touch. Embryonic neural development occurs normally in homozygotes. The volume of DA neurites is significantly diminished in homozygous larvae, whereas the neuronal somae persist. The neuritic degeneration occurs mostly in the abdominal area of the ventral nerve cord. There is no significant change in the neurite volume of serotonergic neurons or in the volume of the motorneuron subpopulation in these larvae. Manf[Δ96] embryos lacking both maternal and zygotic Manf[+] function develop normally until late stage 16, but show severe defects thereafter; the ventral nerve cord (VNC) becomes overcondensed compared to wild type. At early stage 16, the neuropile of the VNC still resembles that of wild type, but by late stage 17, degradation of axonal membranes is seen, starting at the border of the glia and neuropile. In addition, cell body glial cells appear highly electron dense and contain remnants of cell debris. In the VNC, dying cells with poor and bleached cytoplasm, swollen nuclei and with dilated endoplasmic reticulum and other organelles are seen, which is atypical for conventional apoptosis. The cuticle of these embryos is defective; all cuticular layers are disorganised.
ManfΔ96 has lethal | recessive | larval stage phenotype, suppressible by Hsap\MANFScer\UAS.cPa/Scer\GAL4da.G32
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Not rescued by|
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 1 )|