Wild-type garland cell nephrocytes (GCNs) fuse to form binucleate GCNs in third instar larvae. Ectopic expression of rst^Scer\UAS.cSa in garland cells driven by Scer\GAL4^pros.PMG results in excessive GCN fusion resulting in multinucleate GCN cells in third instar larvae.

Overexpression of rst^Scer\UAS.cSa using Scer\GAL4^hs.2sev results in a rough eye phenotype.

Using Scer\GAL4^MZ1369 to drive transgene expression in neurons and glial cells, overexpression of kirre^Scer\UAS.cRa results in a severe disorganization of all four neuropils of the optic lobe. Of these neuropils, the lamina seems to be least affected, while in some cases the inner optic chiasm between medulla, lobula and lobula plate completely disappear, leaving the impression of a fusion between these three otherwise clearly distinct neuropils.

Expression of rst^Scer\UAS.cSa, under the control of Scer\GAL4^MZ1369, leads to the formation of rough eyes. Pupal eyes show a cell sorting defect, and pupal ommatidia are either fused, or separated by multiple layers of interommatidial precursor cells. Bristle complexes are misplaced. These eyes also contain ommatidia with a single cone cell and one primary pigment cell.

When single inter-ommatidial precursor cells (IPCs) in the developing retina are made rst^Scer\UAS.cSa Scer\GAL4^Act5C.PI (by FLP out), their apical profiles are significantly and stably expanded. Typically, single IPCs fill both a secondary pigment cell niche and the adjacent tertiary pigment cell niche - contacting 5 primary pigment cells. Displaced cells are lost rather than relocated within the retina.

rst^Scer\UAS.cSa, when driven by Scer\GAL4^da.G32 causes embryonic lethality, and induces defects in myoblast fusion: muscles are conspicuously thin and unfused myoblasts are present in large numbers. Some muscles seem to be unable to find their proper attachment sites within the epidermis. When rst^Scer\UAS.cSa is driven by Scer\GAL4^how-24B or Scer\GAL4^twi.PB, neither lethality or a muscle phenotype is seen. Scer\GAL4^69B driven by Scer\GAL4^69B does not cause any obvious phenotypes except for some unfused myoblasts attached to the epidermis still present in stage 16. When rst^Scer\UAS.cSa is driven by Scer\GAL4^Dll-md23 or Scer\GAL4^wg.PM in, fusion competent myoblasts are attracted towards sites of ectopic expression.

Expression of rst^Scer\UAS.cSa under the control of Scer\GAL4^sca-P309 results in clusters of sensilla trichoidea on the antenna where intervening epidermal hairs are absent. Epidermal 'pits' containing 'bunches' of sensilla basiconica and trichoidea are seen and the most extreme cases the entire sacculus fails to form. The total number of sensory founder cells in the antennal disc is comparable to wild type, but the pattern of the founder cells (FCs) is disorganised in animals expressing rst^Scer\UAS.cSa under the control of Scer\GAL4^sca-P309. Many FCs are clustered in some regions, while in others, spacing between adjacent precursors is greatly increased. The pattern of apoptotic nuclei in third larval instar antennal discs is no different from wild type.

Scer\GAL4^hs.2sev and Scer\GAL4^MZ1369 mediated expression causes a strong rough eye phenotype, ommatidial lattice is severely disturbed due to frequent ommatidial fusions and randomised bristle distribution. Scer\GAL4^elav.PLu mediated expression causes no retinal defects.

When expressed under the influence of Scer\GAL4^elav.PLu, the optic lobe (but not the central brain) is severely disordered. In severe cases the posterior retina/lamina fibers and C and T fibers form a common plexus. More anterior lamina/retina fibers form thick bundles. These phenotypes are in common with rst loss of function mutants. Hybrids are viable into the adult stage.