Expression of enScer\UAS.cTa in even segments (but not odd) of the developing embryo, under the control of Scer\GAL4prd.RG1 leads to the fusion of anterior and posterior commissures or to the absence altogether of these commissures. In the latter case, the longitudinal tracts appear thicker. The number of neuronal cells remains unchanged in these embryos, indicated a misrouting phenotype rather than apoptosis.
Expression of enScer\UAS.cTa under the control of Scer\GAL4da.G32, a ubiquitous early driver, leads to axonal pathfinding defects.
Expression of enScer\UAS.cTa under the control of Scer\GAL4sca.PC, which drives expression in the neuroblasts and neurons, leads to axonal pathfinding defects.
Expression of enScer\UAS.cTa under the control of pan-neuronal drivers such as Scer\GAL41407 or Scer\GAL4elav.PLu does not generate any major defect in the overall architecture of the ventral nerve cord. At most, some low penetrance effects (less than 1%) are observed.
enScer\UAS.cTa; Scer\GAL4prd.RG1 embryos have severe cuticle defects.
When enScer\UAS.cTa is expressed under the control of Scer\GAL4byn-Gal4, the border cells of the hindgut (which normally form an anterior and posterior ring at the ends of the hindgut and bilateral strands that connect the two rings) fail to form, except at the posterior border of the large intestine.
When expressed under the influence of Scer\GAL4112-97, abnormal wings and halteres develop. Some of the medial triple row bristles along the anterior wing margin are transformed to posterior type, anterior wing shows outgrowths and venation is abnormal. Anterior effects are similar to those caused by In(2R)vgW. Rare partial transformations of haltere to wing (similar to those caused by In(2R)vgW) occur. When expression is driven by Scer\GAL4en-e16E, surviving flies have wings with normal patterns of veins and bristles in the anterior compartment, but abnormal veins and triple row bristles in the posterior compartment. Some wings had outgrowths while others had anterior transformations that were not accompanied by outgrowths.
Scer\GAL4prd.RG1, enUAS.cTa has embryonic/first instar larval cuticle phenotype, suppressible | partially by exd1
NΔE.UAS, Scer\GAL4byn-Gal4, enUAS.cTa has embryonic hindgut phenotype
NΔE.UAS, Scer\GAL4byn-Gal4, enUAS.cTa has embryonic large intestine phenotype
The severity of cuticle defects seen in enScer\UAS.cTa; Scer\GAL4prd.RG1 embryos is reduced in embryos maternally exd1/exd1 and zygotically exd1/+.
When Dl::NΔECN.Scer\UAS and enScer\UAS.cTa are co-expressed under the control of Scer\GAL4byn-Gal4, the entire large intestine differentiates into boundary cells.