Abstract
Metabolism, growth, and development are intrinsically linked, and their coordination is dependent upon inter-organ communication mediated by anabolic, catabolic, and steroid hormones. In Drosophila melanogaster, the corpora cardiaca (CC) influences metabolic homeostasis through adipokinetic hormone (AKH) signaling. AKH has glucagon-like properties and is evolutionarily conserved in mammals as the gonadotropin-releasing hormone, but its role in insect development is unknown. Here we report that AKH signaling alters larval development in a nutrient stress-dependent manner. This activity is regulated by the locus dg2, which encodes a cGMP-dependent protein kinase (PKG). CC-specific downregulation of dg2 expression delayed the developmental transition from larval to pupal life, and altered adult metabolism and behavior. These developmental effects were AKH-dependent, and were observed only in flies that experienced low nutrient stress during larval development. Calcium-mediated vesicle exocytosis regulates ecdysteroid secretion from the prothoracic gland (PG), and we found that AKH signaling increased cytosolic free calcium levels in the PG. We identified a novel pathway through which PKG acts in the CC to communicate metabolic information to the PG via AKH signaling. AKH signaling provides a means whereby larval nutrient stress can alter developmental trajectories into adulthood.
Highlights
Fundamental to all forms of life is the ability to maintain constancy of the internal milieu, or homeostasis, around precisely defined physiological setpoints (Bernard, 1854; Cannon, 1929)
We investigated a putative role for dg2 in the CC (i.e., CCdg2) as a regulator of adipokinetic hormone (AKH) secretion during early development using the GAL4-UAS binary system (Brand and Perrimon, 1993)
Because AKH precursor-related peptide (APRP) putatively regulates the developmental transitions between larval, pupal, and adult life stages in insects, we investigated the effect of akh > Dcr;dg2-RNAi in AKH single (AKHA) and AKH-APRP double (AKHAP) mutant backgrounds (Clynen et al, 2004; Gàlikovà et al, 2015)
Summary
Fundamental to all forms of life is the ability to maintain constancy of the internal milieu, or homeostasis, around precisely defined physiological setpoints (Bernard, 1854; Cannon, 1929). In Drosophila melanogaster, the stress-responsive neuroendocrine corpora cardiaca (CC) is ideally suited to this task (Vogt, 1946). The CC is the sole site of biosynthesis and secretion of the adipokinetic hormone (AKH), a glucagon-like peptide that mobilizes carbohydrate and lipid energy stores in response to starvation (Kim and Rulifson, 2004; Lee and Park, 2004; Isabel et al, 2005). The CC is functionally homologous to the mammalian pancreatic α cells. Perturbations in haemolymph glucose titers are detected by the CC through changes in the activity of evolutionarily conserved ATP-sensitive potassium (KATP) channels (Kim and Rulifson, 2004). In murine pancreatic α cells, a cGMP-dependent protein kinase (PKG, encoded by cGK1 in mice) negatively regulates glucagon
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