Expression of DopEcRKK111211 under the control of Scer\GAL4da.PU leads to significant resistance to ethanol-induced sedation (the flies take longer to cease all movements upon sedation compared to controls). Using tub-Gal80[ts] to limit the time of RNAi expression to the developmental stage - i.e. before eclosion - does not affect sedation sensitivity in the adults, whereas RNAi knockdown after eclosion does increase resistance to ethanol-induced sedation. The increased resistance to sedation is also observed in flies expressing DopEcRKK111211 under the control of any of these drivers: Scer\GAL4elav.PU, Scer\GAL4ChAT.PU or Scer\GAL4dimm-929 but no significant effect is seen when the RNAi is driven by any of the following: Scer\GAL4c747, Scer\GAL4ple.PU or Scer\GAL4Ilp2.PU.
Males expressing DopEcRKK111211 under the control of Scer\GAL4αTub84B.Switch.PK in the presence of RU486 lack 30-minute courtship memory in a courtship conditioning assay. This defect is not suppressed if the males are fed 0.1mM 20-hydroxy-ecdysone immediately prior to conditioning.
Males expressing DopEcRKK111211 under the control of either Scer\GAL4c747 or Scer\GAL4c739 lack 30-minute courtship memory in a courtship conditioning assay.
Unlike in wild type, female flies expressing DopEcRKK111211 under the control of the pan-neuronal driver Scer\GAL4n-syb.PS do not show an increase in sugar-sensitive proboscis extension reflex (PER) in response to L-Dopa feeding. The same effect is seen when DopEcRKK111211 is expressed in Gr5a gustatory receptor neurons (GRNs) under the control of Scer\GAL4Gr5a.8.5. A greater proportion of flies expressing DopEcRKK111211 under the control of Scer\GAL4Gr5a.8.5 also exhibit a PER following 6 hours of wet starvation.