Post-mating Refractoriness in Drosophila melanogaster Depends Upon Ecdysis Triggering Hormone Signaling

The decision to engage in courtship depends on external cues from potential mates and internal cues related to maturation, health, and experience. Hormones allow such information to be conveyed to distal tissues in a coordinated fashion. Here, we show Ecdysis-Triggering Hormone (ETH) is a regulator of male courtship in Drosophila melanogaster, and critical for mate choice and courtship inhibition after the completion of copulation. Preventing ETH release increases male-male courtship and decreases post-copulation courtship inhibition (PCCI). Such aberrant male courtship behavior in ETH-deficient males appears to be the consequence of inabilityto integrate pheromone cues into decision making. Silencing of ETH receptor (ETHR) in GR32A-expressing neurons leads to reduced ligand sensitivity and elevated male-male courtship. We find OR67D is critical for suppression of courtship after mating, and ETHR silencing in OR67D-expressing neurons, and GR32A-expressing neurons to a lesser degree, elevates post-copulation courtship. Finally, ETHR silencing in the corpus allatum increases post-copulation courtship; treatment of with juvenile hormone analog partially restores normal post-mating behavior. ETH, a stress-sensitive reproductive hormone, appears to coordinate multiple sensory modalities to guide Drosophila male courtship behaviors, especially after mating.

Neuroendocrine Regulation of Reproductive Dormancy in the Fruit Fly Drosophila melanogaster: A Review of Juvenile Hormone-Dependent Regulation

Animals can adjust their physiology, helping them survive and reproduce under a wide range of environmental conditions. One of the strategies to endure unfavorable environmental conditions such as low temperature and limited food supplies is dormancy. In some insect species, this may manifest as reproductive dormancy, which causes their reproductive organs to be severely depleted under conditions unsuitable for reproduction. Reproductive dormancy in insects is induced by a reduction in juvenile hormones synthesized in the corpus allatum (pl. corpora allata; CA) in response to winter-specific environmental cues, such as low temperatures and short-day length. In recent years, significant progress has been made in the study of dormancy-inducing conditions dependent on CA control mechanisms in Drosophila melanogaster. This review summarizes dormancy control mechanisms in D. melanogaster and discusses the implications for future studies of insect dormancy, particularly focusing on juvenile hormone-dependent regulation.

Regulation of Drosophila Long-Term Courtship Memory by Ecdysis Triggering Hormone

Endocrine state is an important determinant of learning and memory in animals. InDrosophila, rejection of male courtship overtures by mated females leads to an aversive response manifested as courtship memory. Here we report that ecdysis triggering hormone (ETH) is an obligatory enabler of long-term courtship memory (LTM). ETH deficiency suppresses LTM, whereas augmented ETH release reduces the minimum training period required for LTM induction. ETH receptor knockdown either in the mushroom body (MB) γ lobe or in octopaminergic dorsal-anterior-lateral (DAL) neurons impairs memory performance, indicating its direct action in these brain areas. Consistent with these findings, brain exposure to ETH mobilizes calcium in MB γ lobe neuropils and DAL neurons. ETH receptor (ETHR) knockdown in the corpus allatum (CA) to create juvenile hormone (JH) deficiency also suppresses LTM, as does knockdown of the JH receptor Met in the MB γ lobe, indicating a convergence of ETH and JH signaling in this region of the brain. Our findings identify endocrine-enabled neural circuit components in the brain that are critical for persistent behavioral changes resulting from aversive social experience.

Identification, Localization in the Central Nervous System and Novel Myostimulatory Effect of Allatostatins in Tenebrio molitor Beetle

Allatostatins (ASTs) are pleiotropic insect neuropeptides that are potent myoinhibitors of muscle contractions. In this study, we identified and immunolocalized peptides from the MIP/AST and PISCF/AST families in the nervous system of a model beetle, Tenebrio molitor. Neurons containing MIPs were immunolocalized in the brains of adults and the ventral nerve cords of larvae, pupae and imagines of this species as well as in the retrocerebral complex. PISCFs were immunolocalized in the ventral nerve cord of all stages as well as the brain of the adult beetle. Faint signals were also observed in the corpus allatum but not in the corpus cardiacum. The results allowed us to deduce the sequences of three neuropeptides belonging to MIP/ASTs, Tenmo-MIP4—NWGQFGXWa, Tenmo-MIP5—SKWDNFRGSWa and Tenmo-MIP6—EPAWSNLKGIWa, and one peptide from the PISCF/AST family, QSRYXQCYFNPISCX. Furthermore, we showed for the first time myostimulatory action of endogenous MIP/ASTs. Tenmo-MIP5 caused dose-dependent stimulation of the contractile activity of the beetle oviduct muscles, showing a sigmoidal curve up to 81.20% at the 10−8 M concentration, and the EC50 value for the myostimulatory effect of this peptide was 8.50 × 10−12 M. This is the first report of myostimulatory action of an endogenous myoinhibitory peptide in insect muscles.

Antagonistic actions of juvenile hormone and 20-hydroxyecdysone within the ring gland determine developmental transitions in Drosophila

In both vertebrates and insects, developmental transition from the juvenile stage to adulthood is regulated by steroid hormones. In insects, the steroid hormone, 20-hydroxyecdysone (20E), elicits metamorphosis, thus promoting this transition, while the sesquiterpenoid juvenile hormone (JH) antagonizes 20E signaling to prevent precocious metamorphosis during the larval stages. However, not much is known about the mechanisms involved in cross-talk between these two hormones. In this study, we discovered that in the ring gland (RG) of Drosophila larvae, JH and 20E control each other’s biosynthesis. JH induces expression of a Krüppel-like transcription factor gene Kr-h1 in the prothoracic gland (PG), a portion of the RG that produces the 20E precursor ecdysone. By reducing both steroidogenesis autoregulation and PG size, high levels of Kr-h1 in the PG inhibit ecdysteriod biosynthesis, thus maintaining juvenile status. JH biosynthesis is prevented by 20E in the corpus allatum, the other portion of the RG that produces JH, to ensure the occurrence of metamorphosis. Hence, antagonistic actions of JH and 20E within the RG determine developmental transitions in Drosophila. Our study proposes a mechanism of cross-talk between the two major hormones in the regulation of insect metamorphosis.