Deletion of at least 10kb, removing the Itp-r83A gene.
Itp-r83A90B.0/+ flies have normal wing structure.
Itp-r83A90B.0/+ 30-day-old adult males display learning defects as they fail to demonstrate significant decrease in courtship activity when paired with an mated unreceptive female but their short-term (60 min) memory is not impaired.
Whole cell patch-clamp recordings of dissociated ommatidia from Itp-r83A90B.0 mutants shows that, after light stimulation, the Shab-mediated light-dependent modulation of the delayed rectifier current is indistinguishable from wildtype controls.
Heterozygous flies show an increased resistance to 1% H2O2 compared to control flies.
Lethality acts in the second larval instar. First to second instar molting is delayed.
Itp-r83A90B.0 heterozygotes recover from butanol-induced adaptation faster than wild-type. The response of homozygous Itp-r83A90B.0/+ animals to all concentrations of ethyl acetate is normal.
Homozygous clones in the retina can result in defects in the mechanosensory bristles of the ommatidia, including duplication and missing and misplaced bristles. Ultrastructurally, the morphology of the photoreceptors in homozygous clones appears completely normal in newly eclosed flies. However, the photoreceptors undergo light-independent degeneration; at 2 weeks after eclosion the first signs of degeneration are seen with a subtle deformity at the base of the rhabdomere membrane, while at 8 weeks after eclosion the photoreceptor cells become filled with sacs of vesicles and finally degenerate.
In whole-cell recordings of photoreceptors from flies in which the entire eye is homozygous for Itp-r83A90B.0, quantum bumps are elicited with a quantum efficiency similar to that of wild type and with a similar latency and amplitude compared to wild type. The time courses of wild-type and mutant quantum bumps are indistinguishable. Light adaptation is unaffected in flies in which the entire eye is homozygous for Itp-r83A90B.0.
Homozygous embryos develop normally and hatch as viable first instar larvae. Lethality of homozygotes begins early in the second instar stage, 72 hours after egg-laying (AEL), and by 112 hours AEL nearly all homozygotes are dead. Homozygotes undergo the first larval moult more slowly than wild-type larvae.
Itpr90B.0/Itpr05616 has abnormal developmental rate phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-178
Itpr90B.0/Itpr05616 has lethal | larval stage phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-178
Itpr90B.0/Itpr05616 has lethal | pupal stage phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-178
Itpr90B.0/Itpr05616 has abnormal developmental rate phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-2080
Itpr90B.0/Itpr05616 has lethal | larval stage phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-2080
Itpr90B.0/Itpr05616 has lethal | pupal stage phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-2080
Itpr90B.0 has abnormal developmental rate | recessive phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-2080
Itpr90B.0 has lethal | larval stage | recessive phenotype, enhanceable by Adcy1rut-2080/Adcy1rut-2080
Itpr90B.0 has abnormal learning | male | adult stage phenotype, non-suppressible by PsnB3/Psn[+]
Itpr90B.0 has abnormal learning | male | adult stage phenotype, non-suppressible by PsnI2/Psn[+]
Scer\GAL4Toll-6-D42, NUCB1NIG.32190R/Itpr90B.0 is a suppressor of abnormal locomotor behavior | adult stage phenotype of Hsap\TARDBPUAS.cHa, Scer\GAL4Toll-6-D42
NUCB1c01508, Itpr90B.0, NUCB1[+] is a suppressor of abnormal locomotor behavior | adult stage phenotype of Hsap\TARDBPUAS.cHa, Scer\GAL4Toll-6-D42
Itpr90B.0/Itp-r83A[+] is a suppressor of visible phenotype of IP3K2wy-74i
Itpr90B.0/Itp-r83A[+] is a suppressor of abnormal memory | male | adult stage | progressive phenotype of PsnB3
Itpr90B.0/Itp-r83A[+] is a suppressor of abnormal memory | male | adult stage | progressive phenotype of PsnI2
Itpr90B.0/Itp-r83A[+] is a non-suppressor of abnormal learning | male | adult stage | progressive phenotype of PsnB3
Itpr90B.0/Itp-r83A[+] is a non-suppressor of abnormal learning | male | adult stage | progressive phenotype of PsnI2
Itpr90B.0/Itpr1664GAL4, Pka-R1BDK.UAS, Scer\GAL4Itpr-1664GAL4 has lethal phenotype
Adcy1rut-2080/Adcy1rut-178, Itpr90B.0 has larval tracheal system phenotype
Adcy1rut-2080, Itpr90B.0 has larval tracheal system phenotype
Adcy1rut-2080, Itpr90B.0/Itpr05616 has larval tracheal system phenotype
Itp-r83A90B.0/+ partially suppresses wing phenotypes seen in IP3K2wy-1/IP3K2wy-1, IP3K2wy-2/IP3K2wy-2 or IP3K2wy-74i/IP3K2wy-74i flies.
The learning defects (measured in a courtship behavior assay) observed in the PsnB3, PsnI2 or the Itp-r83A90B.0 single heterozygote 30 day-old males are not suppressed in either the PsnB3/+;Itp-r83A90B.0/+ or the PsnI2/+;Itp-r83A90B.0/+ double heterozygotes. Combination with a single copy of Itp-r83A90B.0 can however restore the short-term memory defects characteristic for both PsnB3 and PsnI2 aged heterozygote males (both at 30 and 40 days of age).
Double mutants with rut alleles show inability to develop beyond the first larval instar, though some of the larvae show spiracles and mouthparts characteristic of second instars, without having molted. The developmental delay of Itp-r83A90B.0/Itp-r83A1664GAL4 transheterozygotes is not affected by P{UAS-PKA.mC} expression.
Itp-r83A90B.0 partially suppresses the climbing defect of 15-day old Scer\GAL4D42>Hsap\TARDBPScer\UAS.cHa flies.
Itpr90B.0/Itpr05616 is partially rescued by Scer\GAL4hs.PU/ItprUAS.cVa