Expression of ArfGAP1Scer\UAS.cRa under the control of Scer\GAL4Hml.Δ results in third instar larval secondary lymph gland lobe overgrowth. Phenotypes are also seen in the primary lobe; an increased number of mitotically active cells is seen in the cortical zone compared to controls and premature differentiation of prohemocytes into plasmatocytes and crystal cells is observed. The number of niche (posterior signalling center) cells is highly reduced compared to controls.
Expression of ArfGAP1Scer\UAS.cRa under the control of Scer\GAL4Hml.Δ results in endocytic trafficking defects during larval haematopoesis. NICD is trapped in Hrs positive endosomes.
Expression of Gap69CScer\UAS.cRa under the control of Scer\GAL4GMR.PF results in a rough eye phenotype. Rhabdomeres develop normally, and there are at best mild endomembrane defects in the cell body.
Flies expressing Gap69CScer\UAS.cRa under the control of Scer\GAL4GMR.PF and grown in bright light show some defects in rhabdomere structure and some accumulation of endomembranes in the cell body of the photoreceptors.
ArfGAP1UAS.cRa, Scer\GAL4GMR.PF has rhabdomere phenotype, enhanceable by Cds1
ArfGAP1UAS.cRa/Scer\GAL4GMR.PF is an enhancer of rhabdomere phenotype of Cds1
ArfGAP1UAS.cRa/Scer\GAL4GMR.PF is an enhancer of eye photoreceptor cell phenotype of Cds1
Co-expression of Gap69CScer\UAS.cRa partially the rhabdomere defects caused by expression of PldScer\UAS.cRa under the control of Scer\GAL4GMR.PF.
Expression of Gap69CScer\UAS.cRa under the control of Scer\GAL4GMR.PF in a CdsA1 background under bright light illumination results in a dramatic increase in the accumulation of whorls of endomembrane within the cell body, accompanied by poorly formed rhabdomeres.