vnγ4/Df(3L)γ3 stage 13/14 embryos show a reduction in longitudinal glia proliferation compared to wild type (assayed using pHis3 expression).
vnγ4/Df(3L)γ3 embryos have various defects in dMP2 fascicles. At stage 14 this fascicle may be absent altogether, it may fuse with the pCC fascicle, or it may fasciculate with the aCC axon and exit the central nervous system (CNS). Older mutant embryos show defasciculation within the CNS particularly of the second and third longitudinal fascicles. vnγ4/Df(3L)γ3 embryos have reduced numbers of longitudinal (interface) glial cells. The frequency and extent of apoptosis of this cell type is significantly greater than that seen in wild-type measured as either: 1. the percentage of embryos with more than one apoptotic longitudinal glial cell (around 80% for wild-type and 50% for mutant (0.025>p>0.05 by ξ2)); or 2. the overall incidence of apoptosis (p>0.001, Mann-Whitney U test.).
Null allele. Shows strongest midgut phenotype of vn alleles tested. Causes lack of midgut constrictions and failure of elongation of gastric caeca.
In vnγ4/Df(3L)γ3 mutants 50% of the Keilin's organs are missing. Head region is normal. Most die as embryos or larvae, but 5% survive to pupariate, with pupal cases shorter and slimmer than wild type.
Individuals transheterozygous with a vn deletion or with a strong EMS vn mutation exhibit small wings. Transheterozygotes with vnL6 are pupal/pharate adult lethal.