wing, with Scer\GAL430A
Expression of DScer\UAS.cSa when driven by Scer\GAL4zfh2-MS209 results wing hinge deletions.
Expression of DScer\UAS.cSa in embryos under the control of Scer\GAL4Mz1407 causes weak defects in the commissures, mainly thinning of the posterior commissures and thickening of the anterior commissure.
DUAS.cSa, Scer\GAL4insc-Mz1407 has larval ventral nerve cord commissure phenotype, enhanceable by Scer\GAL4insc-Mz1407/vvlUAS.cLa
Co-expression of both DScer\UAS.cSa and vvlScer\UAS.cLa in embryos under the control of Scer\GAL4Mz1407 causes more severe neuropile defects than seen in embryos expressing only DScer\UAS.cSa under the control of Scer\GAL4Mz1407; the longitudinals collapse towards the midline throughout the neuropile (although they do not cross the midline), and in some segments, commissures appear fused.
Scer\GAL4sim.PS/DUAS.cSa partially rescues Dr72/Df(3L)fz-GS1a
When DScer\UAS.cSa is expressed under the control of Scer\GAL4en-e16E in D3/Df(3L)fz-GS1a embryos, significant, though variable rescue of the D3/Df(3L)fz-GS1a hindgut phenotype is seen.
The axonal defects of Dr72/Df(3L)fz-GS1a embryos are rescued in the majority of cases if the embryos are expressing DScer\UAS.cSa under the control of Scer\GAL4sim.PS. The number and location of the midline glia cells is also rescued.
