Male flies silencing Ubqn through expression of UbqndsRNA.Ex2.Scer\UAS in neurons under the control of Scer\GAL4elav-C155 suffer premature death. The flies are born normally, but life-span begins to decline shortly after eclosion and significantly declines by the time the flies are 30 days old. At 50 days, over 70% of control flies are still alive, whereas over 80% of UbqndsRNA.Ex2.Scer\UAS;Scer\GAL4elav-C155 flies are already dead. In contrast, no significant difference in life-span is found in mutant females compared to wild-type.
UbqndsRNA.Ex2.Scer\UAS;Scer\GAL4elav-C155 male flies exhibit severe widespread neurodegeneration compared with wild-type flies. In addition, multilamellar structures are found throughout the brain, and the neuropil contains multiple membrane-bound vacuoles.
Silencing of Ubqn by expression of UbqndsRNA.Ex2.Scer\UAS under the control of Scer\GAL4sd-SG29.1 in wing discs results in three types of phenotypes: (i) loss of the partial L4, L5, entire anterior cross vein and posterior cross vein; (ii) a thickened L3 vein, particularly in the distal portion of the margin area of the wing; (iii) notches in the wing margin. These phenotypes show variable penetrance in male and female flies. Compared with female flies, male UbqndsRNA.Ex2.Scer\UAS;Scer\GAL4elav-C155 flies are semi-lethal. All the male flies and approximately 5% of female flies exhibit all three severe phenotypes. The majority of the female flies (95%) exhibit only a weak phenotype as evidenced by loss of the posterior cross vein and anterior cross vein.
Silencing of Ubqn by expression of UbqndsRNA.Ex2.Scer\UAS in the wing disc under the control of Scer\GAL4e22c leads to loss of the entire posterior cross vein, partial loss of the anterior cross vein, and L5 veins and weakened distal portion of L4 and L3-4 M veins in the posterior portion of the wing.
Silencing of Ubqn by expression of UbqndsRNA.Ex2.Scer\UAS in the wing disc under the control of Scer\GAL4ptc-559.1 results in loss of the entire anterior cross vein, narrowing of the intervein sector between L3 and L4 veins in all flies, compared with wild-type controls.
Silencing of Ubqn by expression of UbqndsRNA.Ex2.Scer\UAS in the developing eye disc under the control of Scer\GAL4GMR.PF does not lead to any detectable eye abnormalities.
Scer\GAL4GMR.PF, Scer\GAL4GMR.PF, UbqndsRNA.Ex2.UAS is an enhancer of increased cell death phenotype of Psn+14.UAS
Scer\GAL4e22c, UbqndsRNA.Ex2.UAS has wing vein L4 phenotype, suppressible | partially by rhove-1/Scer\GAL4e22c
Scer\GAL4e22c, UbqndsRNA.Ex2.UAS has wing vein L5 phenotype, suppressible | partially by rhove-1/Scer\GAL4e22c
Scer\GAL4e22c, UbqndsRNA.Ex2.UAS has wing vein L3 phenotype, suppressible | partially by rhove-1/Scer\GAL4e22c
Scer\GAL4e22c, UbqndsRNA.Ex2.UAS has posterior crossvein phenotype, suppressible | partially by rhove-1/Scer\GAL4e22c
UbqndsRNA.Ex2.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of eye phenotype of Psn+14.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
UbqndsRNA.Ex2.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of interommatidial bristle phenotype of Psn+14.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
UbqndsRNA.Ex2.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF is an enhancer of ommatidium phenotype of Psn+14.UAS, Scer\GAL4GMR.PF/Scer\GAL4GMR.PF
Expression of UbqndsRNA.Ex2.Scer\UAS by Scer\GAL4e22c in a heterozygous rhove-1 background leads to a normal anterior cross vein and partially restored posterior cross vein and L5 vein, while the distal portion of L4 and L3-4 M veins corresponding to the posterior portion of the wing remains weakened, compared with UbqndsRNA.Ex2.Scer\UAS; Scer\GAL4e22c single mutants.
Silencing of Ubqn through co-expression of UbqndsRNA.Ex2.Scer\UAS with Psn+14.Scer\UAS in the developing eye under the control of Scer\GAL4GMR.PF enhances the Psn+14.Scer\UAS-induced rough eye phenotype, leading to an even smaller and rougher eye than that observed with Psn+14.Scer\UAS expression alone. Double mutants exhibit a loss of eye pigmentation, suggesting the loss of pigment cells. RNAi silencing of Ubqn in addition to Psn+14.Scer\UAS overexpression results in a much more severe degenerative phenotype than Psn+14.Scer\UAS single mutants, as evidenced by numerous visible holes (2-5υm in diameter) on a small, rough eye. In addition, the ommatidia are very irregular and mostly fused with very few bristles.