EcR

EcR, short for ecdysone receptor, is a nuclear receptor that mediates the action of ecdysteroids in arthropods, most notably insects. The functional receptor is a heterodimer composed of the Ecdysone Receptor (EcR) and Ultraspiracle (USP), the insect ortholog of RXR. The EcR/USP complex binds to ecdysone response elements in the regulatory regions of target genes in response to the steroid hormone 20-hydroxyecdysone (20E).

EcR belongs to the nuclear receptor superfamily. Upon binding 20E, the EcR/USP complex undergoes conformational changes that promote recruitment of transcriptional coactivators and chromatin remodeling, leading to activation of early response genes such as E74, E75, E78 and the Broad-Complex (BR-C). These early genes initiate a transcriptional cascade that executes molting, metamorphosis and broader developmental programs. The signaling pathway interacts with juvenile hormone signaling to regulate developmental timing and outcomes.

Biological roles of EcR signaling are essential for correct progression through molts and metamorphic transitions. In most species, disruption of EcR signaling—by genetic knockdown, mutation, or pharmacological interference—causes developmental arrest or abnormal progression between larval instars, pupation, and adult formation. EcR expression is widespread in tissues that undergo remodeling during molts, including epidermis and imaginal discs in holometabolous insects.

Structure and evolution: EcR is a member of the nuclear receptor family and features a DNA-binding domain with two C4 zinc fingers and a ligand-binding domain, arranged in a modular architecture typical of steroid receptors. The EcR/USP partnership is a defining feature of insect ecdysteroid signaling, with USP acting as the non-ligand-binding partner that stabilizes DNA binding and transcriptional regulation.