Overexpression of hhN.Scer\UAS (under the regulation of Scer\GAL4en-e16E) results in conversion of tertiary fates (thick, pigmented hair) to ectopic secondary fates (smooth cuticle) on the dorsal epidermis of larvae.
When hhN.Scer\UAS is driven by Scer\GAL4unspecified the anterior wing is affected. Morphology and vein patterns are affected.
Scer\GAL4en-e16E-mediated expression causes grossly enlarged and misshapen wing discs.
Ectopic expression of hhN.Scer\UAS results in very similar phenotypes to those caused by ectopic expression of the full length protein, from hhhs.PI.
When expression is driven by Scer\GAL4en-e16E, ventral cuticle defects include a rectangular rather than a trapezoidal shape for the denticle belts and a loss of denticle diversity, and dorsal cuticle defects include a loss of tertiary and an expansion of secondary cell types. The phenotype is essentially identical to that caused by ubiquitous expression of a full length or N-truncated hh gene product.
Scer\GAL4en-e16E, hhN.UAS has dorsal thick hair phenotype, suppressible by cos2
Scer\GAL4en-e16E, hhN.UAS has embryonic/larval cuticle phenotype, suppressible by cos2
Scer\GAL4unspecified, hhN.UAS has wing vein phenotype, suppressible by fu14
Scer\GAL4unspecified, hhN.UAS has wing | anterior phenotype, suppressible by fu14
The reduction in eye size seen in upd1unspecified/Df(1)os1A2 flies is increased by expression of hhN.Scer\UAS under the control of Scer\GAL4ey.PH and extra bristles are seen in the eye.
Overexpression of hhN.Scer\UAS under the regulation of Scer\GAL4en-e16E, in cos2 mutants fails to convert tertiary fates (thick, pigmented hair) to ectopic secondary fates (smooth cuticle) on the dorsal epidermis of larvae.
Feitz et al.