Abstract
Metamorphosis of Drosophila involves proliferation, differentiation and death of larval tissues in order to form the adult fly. The major steroid hormone implicated in the larval-pupal transition and adult tissue modelling is ecdysone. Previous reviews have draw together studies connecting ecdysone signaling to the processes of apoptosis and differentiation. Here we discuss those reports connecting the ecdysone pulse to developmentally regulated cell cycle progression.
Highlights
ecdysone receptor (EcR)/USP structure and function The major developmental hormone in Drosophila, the steroid hormone 20-hydroxyecdysone, commonly known as ecdysone, is secreted from the prothoracic gland (PG) and plays a major role in regulating imaginal disc development
In the presence of the ecdysone ligand, the appropriate EcR nuclear receptor isoform dimerizes with Ultraspiricle (USP), and the complex is stabilised by the ecdysone ligand to allow efficient binding to the ecdysone response element (EcRE) [17,18] and transcriptional activation of ecdysone-responsive genes [19,20,21,22,23]
Blocking ecdysone pathway signaling using UAS-EcR dominant negative transgenes significantly reduces the number of cells progressing through the cell cycle. As both the UAS-EcRA dominant negative (dN) receptor (EcRAdN) and UAS-EcRBdN block the activation of ecdysone responsive genes, these findings suggest that targets of the ecdysone pathway are required for cell cycle progression in the Drosophila wing imaginal disc
Summary
The studies presented here show that the ecdysone pathway can modulate cell cycle progression in Drosophila by regulating mitogenic pathways. This was surprising given the EcR isoforms are the major mediators of the ecdysone signal, combined with the Maduca Sexta [74,75] and Drosophila studies [76] that have demonstrated a clear requirement for ecdysone in MF progression This lead the authors to propose a novel hormone transduction pathway involving an uncharacterized receptor to explain USP functioning independent of EcR in the eye. As Wg is one of the key developmental signals required for inhibition of cell cycle progression in the wing pouch [30,94,95,98,115], this would be consistent with EcR regulating cell cycle by acting to increase levels of crol transcription, which will in turn decrease levels of Wg signaling (Figure 3). Future studies are aimed to determine whether Crol is a key downstream mediator of EcR signaling and whether it achieves repression of Wg by directly binding the wg promoter to downregulate wg transcription
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