Contains a 1.7kb deletion that uncovers part of the regulatory region, the first exon and part of the first intron.
Imprecise excision of the progenitor insertion, resulting in a deletion of approximately 2.1kb of Sap47 sequence.
Sap47156 mutants exhibit normal sensory detection of odorants and tastants as well as normal motor performance and basic neurotransmission at the neuromuscular junction. However, short-term plasticity is distorted. Sap47156 show stronger depression of synaptic transmission during sustained stimulation and exhibit a significantly lower stead-state amplitude compared to controls.
Sap47156 mutants exhibit a 50% reduction in odorant-tastant learning ability.
Associative function is reduced to approximately 50% of wild-type levels in Sap47156 mutants. The same defect is observed for a two-odor differential conditioning paradigm.
Sap47156 mutants do not differ from wild-type when exposed to amyl acetate or fructose.
Mutant neuromuscular junctions show reliable homeostatic compensation (increase in quantal content) after treatment with philanthotoxin-433 for 10 minutes.
Sap47156 is rescued by Scer\GAL4elav-C155/Sap47RA.UAS
Sap47156 mutants expressing Sap47RA.Scer\UAS under the control of Scer\GAL4elav-C155 regain wild-type levels of associative function.