Nucleotide substitution: G578A, in the intron donor splice site.
G13959415A
G578A
G to A change in donor splice site results in a null mutation.
Ipp1/+ 30-day-old adult males display no learning defects as they show normal decrease in courtship activity when paired with an mated unreceptive female and their short-term (60 min) memory is not significantly impaired.
Mutant flies show mild but reproducible hyperexcitability; they show twitching of the legs when recovering from ether anaesthesia. Post-synaptic evoked responses at the larval neuromuscular junction are several-fold larger than in wild-type controls. This increase is maintained at a range of concentrations of extracellular calcium. The size and number of synaptic boutons and active zones is normal in mutant flies. Mutant synapses have similarly sized pools of readily releasable vesicles and similar rates of recycling as wild-type synapses. The frequency and size of spontaneous end-plate currents is normal. The probability of synaptic vesicle release is enhanced compared to wild-type. Mutant synapses are incapable of maintaining a sustained response to a prolonged stimulus.
Ipp1 has abnormal learning | male | adult stage phenotype, suppressible by PsnB3/Psn[+]
Ipp1/Ipp[+] is a suppressor of abnormal learning | male | adult stage | progressive phenotype of PsnB3
Ipp1/Ipp[+] is a suppressor of abnormal memory | male | adult stage | progressive phenotype of PsnB3
Ipp1/Ipp[+] is a non-suppressor of abnormal learning | male | adult stage | progressive phenotype of PsnI2
Ipp1/Ipp[+] is a non-suppressor of abnormal memory | male | adult stage | progressive phenotype of PsnI2
The learning defects (measured by assessing courtship behavior) observed in the PsnB3, PsnI2 or the Ipp1 single heterozygote 30 day-old males are suppressed in the PsnB3/+;Ipp1/+ but not in the PsnI2/+;Ipp1/+ double heterozygotes. Combination with a single copy of Ipp1 can also restore the short-term memory defects characteristic for both aged PsnB3 and PsnI2 heterozygote males.
