Abstract
extradenticle (exd) and the homeotic selector proteins together establish segmental identities by coordinately regulating the expression of downstream target genes. The inappropriate expression of these targets in exd mutant embryos results in homeotic transformations and aberrant morphogenesis. Here we examine the role of exd in adult development by using genetic mosaics and a hypomorphic exd allele caused by a point mutation in the homeodomain. exd continues to be essential for the specification of segmental identities, consistent with a continuing requirement for exd as cofactor of the homeotic selector proteins. Loss of exd results in the homeotic transformation of abdominal segments to an A5 or A6 segmental identity, the antenna and arista to leg, and the head capsule to dorsal thorax or notum. Proximal leg structures are particularly sensitive to the loss of exd, although exd does not affect the allocation of proximal positional values of the leg imaginal disc. Using heat-shocks to induce expression of a hsp70-exd fusion gene, we show that, in contrast to the homeotic selector genes, ubiquitously high levels of exd expression do not cause pattern abnormalities or segmental transformations.
