Orphan nuclear receptor βFTZ-F1 is required for muscle-driven morphogenetic events at the prepupal–pupal transition in Drosophila melanogaster

Abstract

In Drosophila melanogaster, fluctuations in 20-hydroxyecdysone (ecdysone) titer coordinate gene expression, cell death, and morphogenesis during metamorphosis. Our previous studies have supported the hypothesis that βFTZ-F1 (an orphan nuclear receptor) provides specific genes with the competence to be induced by ecdysone at the appropriate time, thus directing key developmental events at the prepupal–pupal transition. We are examining the role of βFTZ-F1 in morphogenesis. We have made a detailed study of morphogenetic events during metamorphosis in control and βFTZ-F1 mutant animals. We show that leg development in βFTZ-F1 mutants proceeds normally until the prepupal–pupal transition, when final leg elongation is delayed by several hours and significantly reduced in the mutants. We also show that βFTZ-F1 mutants fail to fully extend their wings and to shorten their bodies at the prepupal–pupal transition. We find that βFTZ-F1 mutants are unable to properly perform the muscle contractions that drive these processes. Several defects can be rescued by subjecting the mutants to a drop in pressure during the normal time of the prepupal–pupal transition. Our findings indicate that βFTZ-F1 directs the muscle contraction events that drive the major morphogenetic processes during the prepupal–pupal transition in Drosophila.