A male steroid controls female sexual behaviour in the malaria mosquito

Duo Peng, Evdoxia G. Kakani, Enzo Mameli, Charles Vidoudez, Sara N. Mitchell, Gennifer E. Merrihew, Michael J. MacCoss, Kelsey Adams, Tasneem A. Rinvee, W. Robert Shaw and Flaminia Catteruccia ()
Additional contact information
Duo Peng: Harvard T.H. Chan School of Public Health
Evdoxia G. Kakani: Harvard T.H. Chan School of Public Health
Enzo Mameli: Harvard T.H. Chan School of Public Health
Charles Vidoudez: Harvard Center for Mass Spectrometry
Sara N. Mitchell: Harvard T.H. Chan School of Public Health
Gennifer E. Merrihew: University of Washington
Michael J. MacCoss: University of Washington
Kelsey Adams: Harvard T.H. Chan School of Public Health
Tasneem A. Rinvee: Harvard T.H. Chan School of Public Health
W. Robert Shaw: Harvard T.H. Chan School of Public Health
Flaminia Catteruccia: Harvard T.H. Chan School of Public Health

Nature, 2022, vol. 608, issue 7921, 93-97

Abstract: Abstract Insects, unlike vertebrates, are widely believed to lack male-biased sex steroid hormones1. In the malaria mosquito Anopheles gambiae, the ecdysteroid 20-hydroxyecdysone (20E) appears to have evolved to both control egg development when synthesized by females2 and to induce mating refractoriness when sexually transferred by males3. 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. Here we reveal that these reproductive functions are regulated by distinct sex steroids through a sophisticated network of ecdysteroid-activating/inactivating enzymes. 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. Notably, 3D20E transfer also induces expression of a reproductive gene that preserves egg development during Plasmodium infection, ensuring fitness of infected females. Female-derived 20E does not trigger sexual refractoriness but instead licenses oviposition in mated individuals once a 20E-inhibiting kinase is repressed. 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.

Date: 2022
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DOI: 10.1038/s41586-022-04908-6

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