Abstract
Simple SummaryHormones are important signaling molecules mediating insect reproduction that require specific receptors to transmit their signal across the plasma membrane of target cells. While the receptors many hormones bind to are known, some receptors are “orphans” with unknown ligands. The hormone CNMa was previously found to bind a specific receptor in fruit flies. Two copies of the receptor are found in mosquitoes, but only one gene for the hormone is present. We found that both receptors in the yellow fever mosquito are activated by CNMa. One of the receptors is expressed in mosquito ovaries, which to us implies that the hormone and its receptors may be involved in mosquito reproduction. We further found that injecting the peptide into females reduced the number of eggs that were laid. These experiments suggest that CNMa may be an important factor governing mosquito reproduction.Mosquito reproduction is regulated by a suite of hormones, many acting through membrane-bound receptor proteins. The Aedes aegypti G protein-coupled receptors AAEL024199 (AeCNMaR-1a) and AAEL018316 (AeCNMaR-1b) were identified as orthologs of the Drosophila melanogaster CNMa receptor (DmCNMaR). The receptor was duplicated early in the evolution of insects, and subsequently in Culicidae, into what we refer to as CNMaR-1a and CNMaR-1b. AeCNMaR-1a is only detected in male mosquito antennae while AeCNMaR-1b is expressed at high levels in mosquito ovaries. Using a heterologous cell assay, we determined that AeCNMa activates AeCNMaR-1a with a ~10-fold lower concentration than it does AeCNMaR-1b, though both receptors displayed half maximal effective concentrations of AeCNMa in the low nanomolar range. Finally, we show that injections of AeCNMa into blood-fed mated female Ae. aegypti resulted in fewer eggs laid.
Highlights
Mosquitoes are significant vectors of human pathogens due to their requirement of blood meals to produce successive clutches of eggs
Either CNMaR-1 duplicated prior to the divergence of the Brachycera, and CNMaR-1b was lost in the Brachycera, or the duplication occurred after the split of Culicomorpha from Psychomorpha, but prior to the divergence of the Anopheline and Culicine lineages (Figure 1)
We examined the expression of AeCNMa, AeCNMaR-1a, and AeCNMaR-1b across life stages and in female tissues taken at various times post-blood meal (PBM)
Summary
Mosquitoes are significant vectors of human pathogens due to their requirement of blood meals to produce successive clutches of eggs. JH acts upon the fat body and ovaries to induce competency for the uptake of yolk proteins (vitellogenin) synthesized from digested blood proteins [12]. Insulin-like peptides (ILPs) and ovary ecdysteroidogenic hormone (OEH) are released from the mosquito brain, inducing ecdysteroid production in the ovaries and the expression of serine proteases in the midgut [4,6,9]. Ecdysteroids act on the fat body to stimulate the expression of yolk protein genes, resulting in the production of vitellogenin, which is taken up by the 100–150 developing oocytes in the ovaries [4]. Disruption of any of these signaling pathways blocks the development of oocytes, resulting in reproductive failure [9,10]
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