GENETICS OF ECDYSTEROID-REGULATED CENTRAL-NERVOUS-SYSTEM METAMORPHOSIS IN DROSOPHILA (DIPTERA, DROSOPHILIDAE)

We are interested in identifying members of the generic pathway throug h which 20-hydroxyecdysone (20HE) mediates reorganization of the centr al nervous system (CNS) during metamorphosis. Our entry point is the D rosophila Broad-Complex (BR-C), an early 20HE-inducible locus with thr ee genetic subfunctions, each represented by a lethal complementation group. Our previous analysis of mutants demonstrated that all three BR -C subfunctions are necessary for CNS morphogenesis and one is essenti al for visual system organization. We believe the mutant phenotypes re sult from faulty expression of genes normally regulated by the BRC fam ily of zinc-finger proteins. BRC target genes are predicted to have ex pression patterns and/or mutant phenotypes that partially overlap with those of the BR-C. We have examined two candidate genes, IMP-EI and D eformed (Dfd), to determine their positions relative to BR-C in the ho rmone-regulated pathway of CNS metamorphosis. Identified by Natzle and colleagues on the basis of 20HE-inducibility in imaginal discs, IMP-E I transcripts were also found in a subset of CNS glial cells. Our rece nt experiments show that BR-C expression is spatially and temporally p oised to regulate IMP-EI induction by 20HE. We examined IMP-EI transcr ipt accumulation in larval and prepupal CNS of BR-C lethal mutants rep resenting each of the three complementation groups. In all three cases , IMP-EI induction in the CNS of BR-C mutants was comparable to that o f wildtype and of genetic controls. Thus, activity of any individual B R-C subfunction is not essential for IMP-EI induction. Dfd is a homeot ic selector gene in the Antennapedia complex whose larval CNS expressi on has been shown by others to be restricted to a subset of subesophag eal ganglion cells. We have demonstrated that Dfd mutants manifest a d efect in subesophageal ganglion metamorphosis, namely separation from the thoracic ganglion, indistinguishable from that of BR-C mutants. Ho wever, Dfd transcript accumulation in the CNS appears to be indifferen t to 20HE levels in vivo or in vitro. Alternative models for the genet ic pathways controlling CNS metamorphosis are discussed.