Homozygous adults show a normal proboscis extension response (PER) in response to sucrose alone over a 10,000-fold range of sucrose concentrations. However, the PER in response to 0.1M sucrose in the presence of 1M NaCl is reduced only about 1.3-fold in dpr1 flies, in contrast to wild type, where the PER is reduced 2.7- to 3-fold under these conditions. This indicates a defect in the salt aversion response. Homozygotes show a normal proboscis extension response (PER) to either glucose or fructose alone, but the suppression of the PER to glucose or fructose in the presence of 1M NaCl is reduced in homozygotes compared to controls. Heterozygotes have a normal salt aversion response. dpr1/Df(2R)AA21 adults show a reduced salt-induced suppression of the proboscis extension response to 0.1M sucrose in the presence of 1M NaCl compared to wild-type adults.
Separable from: hdc6705. The P{PZ}dpr1 insertion is separable from a second mutation (hdc6705) that fails to complement mutations in hdc. The hdc6705 mutation causes the defect in phototaxis, while the P{PZ}dpr1 insertion is solely responsible for the mutant gustatory phenotype seen in the original line.
