Amino acid replacement: term978N.
Mutation in the wild-type stop codon that adds an extra 104 residues to the protein.
term978N
The reported stop to Asn amino acid change (TAA to AAT/C) requires substitution at two positions in the codon.
NMJ bouton | larval stage (with wnd1)
wnd2 mutants exhibit wild-type synapse size.
wnd1/wnd2 is a suppressor | partially of lethal | dominant phenotype of Scer\GAL4elav.PU, SkpAGD65, fafUAS.cUa
wnd1/wnd2 is a suppressor | partially of abnormal neurophysiology | larval stage phenotype of SkpAGD65
wnd[+]/wnd2 is a suppressor | partially of abnormal neuroanatomy | third instar larval stage phenotype of shotVV/shot3
wnd3/wnd2 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of shotVV/shot3
wnd[+]/wnd2 is a suppressor of abnormal neuroanatomy phenotype of Scer\GAL4elav-C155, sggA81T.UAS
wnd1/wnd2 is a suppressor of abnormal neurophysiology phenotype of hiwND8
wnd1/wnd2 is a suppressor | partially of NMJ bouton | maternal effect | larval stage phenotype of SkpAGD65
wnd1/wnd2 is a suppressor | partially of embryonic/larval neuromuscular junction | maternal effect | larval stage phenotype of SkpAGD65
wnd[+]/wnd2 is a suppressor | partially of NMJ bouton | increased number | third instar larval stage phenotype of shotVV/shot3
wnd3/wnd2 is a suppressor of NMJ bouton | increased number | third instar larval stage phenotype of shotVV/shot3
wnd[+]/wnd2 is a suppressor of synapse phenotype of Scer\GAL4elav-C155, sggA81T.UAS
wnd1/wnd2 is a suppressor of neuromuscular junction phenotype of Scer\GAL4elav-C155, fafEP381
wnd1/wnd2 is a suppressor of bouton phenotype of Scer\GAL4elav-C155, fafEP381
wnd1/wnd2 is a suppressor of neuromuscular junction phenotype of hiwND8
A wnd2/+ background completely abolishes the synapse growth seen through sggA81T.Scer\UAS expression pan-neuronally under the control of Scer\GAL4elav-C155.
hiwND8; wnd1/wnd2 mutants are not significantly different from wild-type, indicating complete suppression of hiwND8.
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.