Coexpression of shg^ex.Scer\UAS with shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs}, under the control of Scer\GAL4^hs.2sev, does not rescue the shg^{dCR3h.Scer\UAS.T:Avic\GFP-rs} ommatidial rotational defects.

When shg^ex.Scer\UAS is driven by Scer\GAL4^da.G32 mutant embryos exhibit cuticle phenotypes of variable expressivity. Phenotypes range from, head defects, ventral holes to severe reduction of the entire epidermis. When shg^ex.Scer\UAS is driven by Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}, 12% of embryos exhibit defects in nuclear localisation and cellularisation in the blastoderm stage. In these embryos, nuclei are distributed unevenly, often leaving gaps at the surface. This mislocalisation starts before cellularisation - embryos in cell cycles 12 and 13 are seen with nuclei that have irregularities in horizontal patterning and in their distance from the egg membrane. This phenotype increases in severity and become compounded by defective cellularisation during cell cycle 14. Cell membranes form irregularly and are lacking completely around many nuclei. These embryos fail to develop any further. Those that do not exhibit a phenotype at the blastoderm stage, exhibit phenotypes in mitosis and neurulation. In these embryos mitosis is disrupted as early as stage 6. Mitosis of the dorsal ectoderm is de-synchronised compared to wild type, and the average cell cycle length seems to be reduced. The spindle orientation of dividing neuroectodermal cells is also disrupted in stages 8-9. Cells in the surface ectoderm frequently exhibit vertical mitotic spindles. In addition, spindle orientation in neuroblasts is randomised, resulting in neurons and ganglion mother cells covering neuroblasts on all sides. Phenotypes are also seen in half of shg^ex.Scer\UAS, Scer\GAL4^{mat.αTub67C.T:Hsim\VP16} embryos during gastrulation. The ventral furrow does not invaginate, or invaginates only partially. Cells prematurely lose their monolayered epithelial character and form double or triple layers of rounded cells that lack regular zonula adherens. Sometimes embryos exhibit a "exogastrulation"-like behaviour, usually at the posterior pole. In many gastrulation stage embryos, mesodermal cells manage to translocate inside the embryo. however the ventral furrow never fully closes, leaving wide stretches of mesoderm exposed at the ventral surface.

Expression of shg^ex.Scer\UAS in early third instar brains, under control of Scer\GAL4^hs.PH following a heat pulse, causes a reduction in brain size compared with wild-type brains and loss of proximal axon tracts. In the more extreme cases, neuroblasts have reduced mitotic activity leading to a reduction in numbers of secondary neurons. This is accompanied by the loss of the centroanterior protocerebral tract. Additionally, shg^ex.Scer\UAS-expressing neuroblasts are clustered closely together, while wild-type neuroblasts are relatively evenly-spaced over the surface of the central brain.

Expression of shg^ex.Scer\UAS, under the control of the glial cell-specific driver Scer\GAL4^gcm-rA87.C in the second instar brain, also leads to a decrease in the size of larval brains with reduced neuronal proliferation, which appears to be due to a reduction in mitosis.

Expression of shg^ex.Scer\UAS, under the control of the neuron-specific Scer\GAL4^elav-C155 in the third instar brain, leads to the ectopic location of neuroblasts; these can be found deep in the cortex of mutant brains, whereas neuroblasts are always located at the brain surface of wild-type larvae. Additionally, proximal axon tracts travel at various angles relative to the brain surface in the mutants, instead of following a straight radial course, as in wild type. Expression of shg^ex.Scer\UAS, driven by Scer\GAL4^hs.PH following a heat pulse in the second instar, disrupts the neuropile and cortex glia. The neuropile glial sheath is interrupted and there is intermixing of neuronal stomata and axons at the cortex-neuropile boundary.

When shg^ex.Scer\UAS is expressed in mid third instar brains under the control of Scer\GAL4^nrv2.PS, the trophospongium is severely reduced and neurons that are usually only found in superficial chambers of this structure can be found throughout the cortex. Additionally, the glial sheath surrounding the neuropile is uneven and full of gaps and many cortex glial cell bodies appear to be more rounded and bulky than in wild-type brains.