Flies expressing Pink1dsRNA.Scer\UAS.cWa under the control of Scer\GAL4GMR.PF at room temperature have a mutant eye phenotype characterised by pigmentation deficits and bristle loss. The flies also have black lesions in the eyes.
Adult brains of 1 day-old flies expressing Pink1Scer\UAS.dsRNA.cWa under the control of Scer\GAL4elav.PLu show little difference in the number and distribution of dopaminergic (DA) neurons compared to controls. In contrast, mutant flies show a dramatic reduction in DA neuron number at 10 days of age, compared to age-matched controls: significant neuronal loss is seen in most DA neuron clusters including in the PAL, PPM1/2, PPM3, PPL2 and less so in PPL1, although the number of DA neurons in the VUM regions are not significantly affected. (Staining of serotonergic neurons shows little difference between Pink1Scer\UAS.dsRNA.cWa-expressing and control flies.) A similar loss of DA neurons is seen in the adult brains of flies expressing Pink1Scer\UAS.dsRNA.cWa under the control of Scer\GAL4Ddc.PL.
Expression of Pink1Scer\UAS.dsRNA.cWa under the control of Scer\GAL4GMR.PF or Scer\GAL4elav.PLu results in age-dependent progressive ommatidial degeneration manifested in black lesions in the adult eyes. These eyes are also 'rough', with disorganized interommatidial bristles. Pink1Scer\UAS.dsRNA.cWa, Scer\GAL4GMR.PF pupal eyes (observed at 44 hours APF) exhibit morphologically disrupted ommatidia, increased and misorientated mechanosensory bristle groups, disorganized and enlarged pigment cells, and a significant loss of photoreceptor neurons compared to controls.
Treatment with antioxidants (recombinant SOD1 protein or vitamin E) inhibits the ommatidial degeneration defects in flies expressing Pink1Scer\UAS.dsRNA.cWa under the control of Scer\GAL4GMR.PF.