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Ecdysis Triggering Hormone: A Multifunctional Peptide Regulator of Reproductive Physiology in Yellow Fever Mosquito Aedes aegypti


During development, insects perform ecdysis behaviors required for shedding of old cuticle at the end of each molt. These behaviors are orchestrated by circulating peptides known as ecdysis triggering hormones (ETHs). Secreted by endocrine Inka cells, ETH acts on target neurons in the CNS via two GPCR isoforms (ETHR-A and ETHR-B) to recruit downstream peptide signaling cascades. Recent work on Drosophila melanogaster shows that Inka cells and transcripts encoding ETH and ETHR receptors persist through metamorphosis into adulthood, a period during which no ecdysis occurs. This suggests possible regulation of reproductive functions by ETH.

Many studies about reproductive physiology have been conducted in the yellow fever mosquito Aedes aegypti. In Aedes species, egg development proceeds through previtellogenic and vitellogenic phases. During previtellogenesis, the follicles, which are about 45 µm long at eclosion, grow to 100-110 µm. The previtellogenic phase controlled by Juvenile hormone (JH) begins at eclosion and is completed in ~60 hr, leading to competence for vitellogenesis, which is triggered by the blood meal. During vitellogenesis, the fat body produces the yolk protein precursor vitellogenin. At the same time, oocytes accumulate vitellogenin to form protein yolk, leading to egg maturation.

The main goal of my research is to demonstrate and characterize ETH signaling in adult mosquitoes, to study endocrine cross talk between the hormones JH, ETH and ecdysteroids, and to establish their functional significance in mosquito reproductive physiology, which will contribute to a more complete understanding of mosquito reproduction. Here I report that ecdysone (20E)-dependent ETH signaling persists during the adult stage of the yellow fever mosquito (Aedes aegypti). I find that ETH functions as an obligatory allatotropin to promote juvenile hormone (JH) production and previtellogenesis. ETH signaling deficits lead to reductions of follicle size and egg production by producing JH deficiency. My findings indicate that the ecdysteroids, ETH, and JH function as an endocrine network essential for reproductive success in Aedes aegypti.

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