We also profiled ecdysteroids in newly eclosed (<1 day old) males and females and detected 3D20E and 3D20E22P only in the MAGs E, 20E and 20E22P were present in both sexes (Extended Data Fig. No detectable levels of 3D20E22P or 3D20E were found in blood-fed females, although E and 20E (and low levels of 20E22P) were detected in the rest of the body, as expected 11, and in the lower reproductive tract (LRT Extended Data Fig. The HPLC–MS/MS signal intensity of 3D20E22P was two orders of magnitude higher than that of its dephosphorylated form 3D20E and three orders of magnitude higher than that of E and 20E (Fig. ![]() However, samples were dominated by an oxidized, phosphorylated steroid consistent with the chemical formula 3-dehydro-20E-22-phosphate (3D20E22P) 12 (Fig. Using high-performance liquid chromatography coupled with tandem mass spectrometry (HPLC–MS/MS) rather than the less-specific methods previously used 7, 10, 11, we detected ecdysone (E) and 20E in this tissue, confirming previous results. gambiae males, searching for possible modified steroids. We set out to determine the full composition of steroid hormones in the male accessory glands (MAGs) of sexually mature A. 9), male-biased steroids have not been identified in insects, to the best of our knowledge. However, whereas vertebrates have multiple classes of largely dimorphic steroid hormones such as oestrogens and androgens (reviewed in ref. ![]() gambiae males transfer a modified, male-specific ecdysteroid that activates signalling cascades in the female reproductive tract, leading to mating refractoriness. Indeed, if sexual refractoriness were to be triggered by female-produced 20E, this would cause sterility in individuals that blood feed as virgins, which is a highly common behaviour among these mosquitoes 5.Ī possible explanation is that A. However, the manner in which females integrate signals originating from two different ecdysteroid sources (male transferred and blood feeding induced) without impairing their own ability to mate is poorly understood. This is particularly notable because, in these species, 20E is also produced by females after every blood meal, whereby 20E drives the oogenetic cycles (reviewed in ref. The ability of males to synthesize and transfer 20E has evolved specifically in a subset of Anopheles species from the Cellia subgenus 7, which populates Africa and comprises the most dangerous malaria vectors, including Anopheles gambiae 5. Studies have suggested that the trigger of refractoriness to further mating is 20-hydroxyecdysone (20E) 3, a steroid hormone better known as a regulator of molting cycles during larval stages 6. The mating biology of these mosquitoes is a particularly attractive target for novel malaria control interventions because females mate only once 5 rendering this single mating event sterile would have tremendous potential for reducing field mosquito populations.įemales lose their sexual receptivity after receiving high titres of steroid hormones from males. Malaria cases and deaths are once more on the rise 4 owing to several factors including widespread insecticide resistance in Anopheles mosquitoes, which are the only vectors for human malaria parasites. Identifying this male-specific insect steroid hormone and its roles in regulating female sexual receptivity, fertility and interactions with Plasmodium parasites suggests the possibility for reducing the reproductive success of malaria-transmitting mosquitoes. Female-derived 20E does not trigger sexual refractoriness but instead licenses oviposition in mated individuals once a 20E-inhibiting kinase is repressed. ![]() ![]() Notably, 3D20E transfer also induces expression of a reproductive gene that preserves egg development during Plasmodium infection, ensuring fitness of infected females. We identify a male-specific oxidized ecdysteroid, 3-dehydro-20E (3D20E), which safeguards paternity by turning off female sexual receptivity following its sexual transfer and activation by dephosphorylation. Here we reveal that these reproductive functions are regulated by distinct sex steroids through a sophisticated network of ecdysteroid-activating/inactivating enzymes. Because egg development and mating are essential reproductive traits, understanding how Anopheles females integrate these hormonal signals can spur the design of new malaria control programs. In the malaria mosquito Anopheles gambiae, the ecdysteroid 20-hydroxyecdysone (20E) appears to have evolved to both control egg development when synthesized by females 2 and to induce mating refractoriness when sexually transferred by males 3. Insects, unlike vertebrates, are widely believed to lack male-biased sex steroid hormones 1.
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