Abstract
The asense (ase) gene of the achaete-scute complex (AS-C) is expressed in the precursors of all adult sensory organs (SOs), the sensory mother cells (SMCs) and in their immediate progeny. Its deletion causes the loss of some SOs and the abnormal differentiation of part of the remaining ones. These defects, which include malformations of the external part of the SOs, duplication of the innervating neuron etc, are enhanced by the haploid condition for the other AS-C genes and are corrected by an ase transgene. We conclude that ase participates, in combination with other members of the AS-C, in implementing the neural program of differentiation of the SMCs. ase also has a proneural function that participates in the singling out of the SMCs that give rise to the recurved bristles of the anterior wing margin. The proneural potential of ase is shown, in addition, by the generation of SOs induced by the generalized expression of an ase gene driven by a hsp70 promoter.
