Steroid hormones control metabolism, reproduction, and development in many organisms and have been linked to numerous human health problems. Steroids often control major transitions in the life cycle, regulating distinct cell responses in a stage-specific manner. Despite their global importance in development, relatively little is known about how steroid hormones control such stage-specific responses.

One of the most dramatic life-cycle transitions driven by steroids is the metamorphosis of insects, in which there is a wholesale transformation of the larva into the adult. In Drosophila, metamorphosis is triggered by pulses of the steroid hormone 20-OH ecdysone (ecdysone). A complex of ecdysone bound to its nuclear receptor, a heterodimer of the ecdysone receptor (EcR) and the RXR ortholog Ultraspiracle (Usp), directly activates a small number of primary response genes, including Eip93F (Ecdysone induced protein at 93F, hereafter called E93) which in turn regulate many secondary response genes that function more directly in controlling cell fate. The role of ecdysone signaling in early events of metamorphosis, such as the death of larval cells and the morphogenesis of adult structures, has been studied extensively. However, mechanisms underlying the control of adult cell fates by ecdysone have been poorly characterized.

In adult cells, many genes seem to undergo a change in their response to specific signaling systems or transcription factors during metamorphosis. Such transitions are most clearly illustrated by recent work showing that targets of the Hox protein Ubx change dramatically at the prepupal and pupal stages. In addition, studies of wing venation and heart remodeling, and patterning during metamorphosis in the wing, eye, palp, and abdominal cuticle indicate similar shifts. Such global changes in target responsiveness likely explain how the same signaling systems and identity genes used to pattern the larva during embryogenesis are redeployed during metamorphosis to pattern the adult; however, it is not known how such transitions are controlled.

We have identified the ecdysone response gene E93 as a key determinant of target gene responsiveness during the pupal phase of metamorphosis. E93 is known to be required for the death of larval tissues, such as the midgut and salivary glands early in metamorphosis, and has been considered a dedicated regulator of cell death. However, we find that E93 is expressed extensively in imaginal (adult) cells during pupal development and is required for the patterning of many adult structures at this time.