When expressed at high level (two copies of RhoGAP93BScer\UAS.cHa and two copies of Scer\GAL4elav.PLu, or three copies of RhoGAP93BScer\UAS.cHa and one of Scer\GAL4elav.PLu) a range of defects are observed. Multiple ectopic crosses of the longitudinal axons at the midline are seen, and the whole axon scaffold is altered, causing a thickening of the commissures and thinning of longitudinal connectives. Some embryos show an axon outgrowth defect, in which multiple longitudinal axon pathways fail to extend.
RhoGAP93BUAS.cHa, Scer\GAL4elav.PLu is an enhancer of medial longitudinal fascicle phenotype of Rac1N17.UAS, Scer\GAL4elav.PLu
RhoGAP93BUAS.cHa, Scer\GAL4GMR.PF is a suppressor of ommatidium phenotype of Rac1UAS.cLa, Scer\GAL4GMR.PF
RhoGAP93BUAS.cHa, Scer\GAL4GMR.PF is a suppressor of photoreceptor neuron phenotype of Rac1UAS.cLa, Scer\GAL4GMR.PF
RhoGAP93BUAS.cHa, Scer\GAL4GMR.PF is a non-suppressor of photoreceptor neuron phenotype of Rho1UAS.cMa, Scer\GAL4GMR.PF
RhoGAP93BUAS.cHa, Scer\GAL4GMR.PF is a non-suppressor of ommatidium phenotype of Rho1UAS.cMa, Scer\GAL4GMR.PF
When RhoGAP93BScer\UAS.cHa is driven by RhoGAP93BScer\UAS.cHa in a sli1/+, robo5/+ background, the axon scaffold of the ventral midline is severely disrupted. The ectopic crossing defect see at low frequency in sli1/+, robo5 embryos is enhanced.
When RhoGAP93BScer\UAS.cHa is driven by Scer\GAL4elav.PLu in a fraunspecified background no midline crossing defects are seen. When RhoGAP93BScer\UAS.cHa and fraScer\UAS.cKa are driven by Scer\GAL4elav.PLu no midline crossing defects are seen. When RhoGAP93BScer\UAS.cHa is driven by Scer\GAL4elav.PLu in a Ptp69Dunspecified;Ptp10Dunspecified background no midline crossing defects are seen. When RhoGAP93BScer\UAS.cHa is driven by Scer\GAL4elav.PLu in a Ptp69D4;Ptp10Dunspecified background no midline crossing defects are seen.
RhoGAP93BUAS.cHa/Scer\GAL4GMR.PF partially rescues RhoGAP93BRNAi.UAS.cBa