eye | progressive, with Scer\GAL4GMR.PF
Expression of httdsRNA.Scer\UAS under the control of Scer\GAL4insc.PU results in mitotic spindle positioning defects in third instar larval neuroblasts: in contrast to wild-type controls, a significant proportion of cells show spindles with the angle between centrosomal pole and center of the mira protein crescent higher than the 15[o].
Newly hatched flies expressing Scer\GAL4GMR.PF>httdsRNA.Scer\UAS have normal eyes. These flies show a progressive loss of pigmentation associated with a rough eye phenotype. The rough eye phenotype is characterised by abnormal ommatidial arrays.
When httdsRNA.Scer\UAS is driven by Scer\GAL4Appl.G1a larvae exhibit defects characteristic of axonal transport problems (organelles accumulate within larval nerves) as well as a small amount of cell death in the larval brain. When httdsRNA.Scer\UAS is driven by Scer\GAL4GMR.PS, a rough eye phenotype is seen. This phenotype progresses over time, causing severe problems of morphology and pigmentation, leading to dark areas indicative of death. Large holes are visible in the most lateral part of the lamina.
Scer\GAL4GMR.PF, httRNAi.UAS has visible | progressive phenotype, suppressible by Hsap\HTTQ0.UAS, Scer\GAL4GMR.PF
Scer\GAL4Appl.G1a, httRNAi.UAS has axon | larval stage phenotype, enhanceable by Klc[+]/Klc8ex94
Scer\GAL4Appl.G1a, httRNAi.UAS has axon | larval stage phenotype, enhanceable by Khc[+]/Khc9
Scer\GAL4Appl.G1a, httRNAi.UAS has axon | larval stage phenotype, non-enhanceable by Df(2R)k10408/+
Scer\GAL4Appl.G1a, httRNAi.UAS has axon | larval stage phenotype, non-enhanceable by Df(3L)GN24/+
Scer\GAL4GMR.PF, httRNAi.UAS has eye | progressive phenotype, suppressible by Hsap\HTTQ0.UAS, Scer\GAL4GMR.PF