UASt regulatory sequences drive expression of an RNAi construct that specifically targets the Dp186 isoform.
Expression of DysdsRNA.mub.UAS in either presynaptic cholinergic neurons (under the control of Scer\GAL4ChAT.7.4) or in the postsynaptic motor neurons aCC/RP2 (under the control of Scer\GAL4eve.RN2) significantly increases synaptic currents (more so under the control of Scer\GAL4eve.RN2).
DysRNAi.Dp186.UAS, Scer\GAL4eve.RN2 has abnormal neurophysiology phenotype, non-enhanceable by witB11/witA12
DysRNAi.Dp186.UAS, Scer\GAL4eve.RN2 has abnormal neurophysiology phenotype, non-suppressible by witB11/witA12
DysRNAi.Dp186.UAS/Scer\GAL4eve.RN2 is a suppressor of abnormal neurophysiology | heat sensitive phenotype of ChATts2
Overexpression of DysdsRNA.mub.Scer\UAS post-synaptically under the control of Scer\GAL4eve.RN2 suppresses the reduced synaptic currents found in Chats2 mutant second instar larvae raised at 18[o]C.
Post-synaptic expression of DysdsRNA.mub.Scer\UAS under the control of Scer\GAL4eve.RN2 in a witA12/witB11 background increases the synaptic current as in a wild-type background.