G173E | wnd-PA; G173E | wnd-PB; G173E | wnd-PC; G146E | wnd-PD
The mutation was mapped to G173 because there is no G at position 172 in the reference sequence. Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.
The synaptic overgrowth phenotype (increase in bouton number) seen at the neuromuscular junction in larvae derived from homozygous SkpAGD65 females is significantly (but not completely) suppressed by wnd1/wnd2.
A wnd1 heterozygous background partially suppresses the high levels of autophagy and bouton number found upon expression of Atg1Scer\UAS.cSa under the control of Scer\GAL4elav.PLu. A wnd1 homozygous background completely suppresses the neuromuscular junction overgrowth phenotype.
wnd1/wnd2 mutants do not suppress the hiwND8 defect in quantal size: both the amplitude and the frequency of spontaneous miniature events in the hiwND8; wnd1/wnd2 double mutant are similar to wild-type. In contrast, the evoked potentials of the double mutant are only modestly increased, and this is due entirely to the increased quantal size. The quantal content, calculated as the excitatory junction potential (EJP) amplitude divided by the miniature EJP (mEJP) remains the same between hiwND8 and hiwND8; wnd1/wnd2 double mutants. Therefore wnd does not suppress the primary defect in hiwND8 synaptic function, the reduced number of vesicles released by the nerve.