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.
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.