Abstract
ABSTRACTSteroid hormones influence diverse biological processes throughout the animal life cycle, including metabolism, stress resistance, reproduction, and lifespan. In insects, the steroid hormone, 20-hydroxyecdysone (20E), is the central hormone regulator of molting and metamorphosis, and plays roles in tissue morphogenesis. For example, amnioserosa contraction, which is a major driving force in Drosophila dorsal closure (DC), is defective in embryos mutant for 20E biosynthesis. Here, we show that 20E signaling modulates the transcription of several DC participants in the amnioserosa and other dorsal tissues during late embryonic development, including zipper, which encodes for non-muscle myosin. Canonical ecdysone signaling typically involves the binding of Ecdysone receptor (EcR) and Ultraspiracle heterodimers to ecdysone-response elements (EcREs) within the promoters of responsive genes to drive expression. During DC, however, we provide evidence that 20E signaling instead acts in parallel to the JNK cascade via a direct interaction between EcR and the AP-1 transcription factor subunit, Jun, which together binds to genomic regions containing AP-1 binding sites but no EcREs to control gene expression. Our work demonstrates a novel mode of action for 20E signaling in Drosophila that likely functions beyond DC, and may provide further insights into mammalian steroid hormone receptor interactions with AP-1.
Highlights
Dorsal closure (DC) of the Drosophila embryo is a developmental wound-healing event in which a hole in the dorsal epidermis, occupied by a transient epithelium, the amnioserosa, is closed by migration of the epidermal flanks
This mechanism is conserved in DC where the leading edge epidermal cells secrete Decapentaplegic (Dpp), a transforming growth factor β (TGF-β) ligand that activates a signaling pathway in the amnioserosa through the receptors Thickveins (Tkv) and Punt, which are required for correct amnioserosa morphogenesis (Fernández et al, 2007; Wada et al, 2007; Zahedi et al, 2008)
Dpp signaling to the amnioserosa leads to 20E production, which is required for correct morphogenesis of the tissue during DC Given that Dpp signaling to the amnioserosa is required for morphogenesis during DC, and that 20E required for DC is produced in the amnioserosa, we tested the hypothesis that Dpp regulated 20E production
Summary
Dorsal closure (DC) of the Drosophila embryo is a developmental wound-healing event in which a hole in the dorsal epidermis, occupied by a transient epithelium, the amnioserosa, is closed by migration of the epidermal flanks (reviewed in Harden, 2002). A recurring finding in studies of wound healing and developmental epithelial closures is that cells occupying the hole contribute to closure by contracting in response to signaling from the hole margin by transforming growth factor β (TGF-β) superfamily ligands (reviewed in Belacortu and Paricio, 2011) This mechanism is conserved in DC where the leading edge epidermal cells (i.e. the dorsal-most epidermal, DME, cells) secrete Decapentaplegic (Dpp), a TGF-β ligand that activates a signaling pathway in the amnioserosa through the receptors Thickveins (Tkv) and Punt, which are required for correct amnioserosa morphogenesis (Fernández et al, 2007; Wada et al, 2007; Zahedi et al, 2008). The amnioserosa is a major source of 20E during embryogenesis, and mutants of the Halloween group of genes, which encode enzymes in the 20E biosynthetic pathway, display DC defects (Chavez et al, 2000; Giesen et al, 2003; Kozlova and Thummel, 2003; Niwa et al, 2010; Ono et al, 2006)
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