Chapter 7 - Molecular mechanisms regulating hormone production and action

Abstract

Prothoracicotropic hormone and insulin-like peptides, which stimulate ecdysone production, act through tyrosine kinase transmembrane receptors. Most prothoracicostatic hormones, the allatotropins and allatostatins that modulate juvenile hormone (JH) production, and ecdysis and tanning hormones, act through G protein-coupled transmembrane receptors. The receptors of ecdysone/20-hydroxyedcysone (20E) and JH are intracellular, belonging to the nuclear receptor and to the basic helix-loop-helix/Per-Arnt-Sim (bHLH/PAS) families, respectively. The 20E signaling pathway is based on a cascade of gene expression initiated by the ecdysone receptor, which activates early genes, like Broad complex (BR-C) and E93, which in turn activate late genes. BR-C promotes wing development in hemimetabolan insects and determines the pupal stage in holometabolans. E93 triggers metamorphosis in hemimetabolan and holometabolan insects. The JH signaling pathway starts with the JH receptor Methoprene tolerant, which induces the expression of Krüppel homolog 1 (Kr-h1), whose gene product represses E93, thus preventing metamorphosis, a regulatory axis known as MEKRE93 pathway. E93 not only functions as a transcription factor but also modulates chromatin accessibility, thus acting at an upper regulatory layer. The MEKRE93 pathway exemplifies the interactions between 20E and JH, but there are other examples of interaction, like the modulatory effect of JH on the expression of 20E-dependent genes. The TGF-β signaling pathway is also important, as it can influence JH synthesis and metamorphosis. Importantly, the antimetamorphic action of JH does not operate in early juvenile stages. The search for the mechanisms that confer competence to metamorphose in late stages is ongoing.