ArticlePLoS pathogens2020
A mating-induced reproductive gene promotes Anopheles tolerance to Plasmodium falciparum infection.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Dual functions of the Aedes aegypti ecdysone receptor in dengue virus replication and reproduction control.Parasites & vectors · 2026Article
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- Revisiting the paradigm of anhematophagy in male mosquitoes.bioRxiv : the preprint server for biology · 2024Article
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- Precise coordination between nutrient transporters ensures fertility in the malaria mosquito Anopheles gambiae.PLoS genetics · 2024Article
- Evolutionary modelling indicates that mosquito metabolism shapes the life-history strategies of Plasmodium parasites.Nature communications · 2023Article
- Using an antimalarial in mosquitoes overcomes Anopheles and Plasmodium resistance to malaria control strategies.PLoS pathogens · 2022Article
- Plasmodium development in Anopheles: a tale of shared resources.Trends in parasitology · 2022Review
- Review
- 20-Hydroxyecdysone (20E) signaling as a promising target for the chemical control of malaria vectors.Parasites & vectors · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 3 countries.
Funding
Abstract
Anopheles mosquitoes have transmitted Plasmodium parasites for millions of years, yet it remains unclear whether they suffer fitness costs to infection. Here we report that the fecundity of virgin and mated females of two important vectors-Anopheles gambiae and Anopheles stephensi-is not affected by infection with Plasmodium falciparum, demonstrating that these human malaria parasites do not inflict this reproductive cost on their natural mosquito hosts. Additionally, parasite development is not impacted by mating status. However, in field studies using different P. falciparum isolates in Anopheles coluzzii, we find that Mating-Induced Stimulator of Oogenesis (MISO), a female reproductive gene strongly induced after mating by the sexual transfer of the steroid hormone 20-hydroxyecdysone (20E), protects females from incurring fecundity costs to infection. MISO-silenced females produce fewer eggs as they become increasingly infected with P. falciparum, while parasite development is not impacted by this gene silencing. Interestingly, previous work had shown that sexual transfer of 20E has specifically evolved in Cellia species of the Anopheles genus, driving the co-adaptation of MISO. Our data therefore suggest that evolution of male-female sexual interactions may have promoted Anopheles tolerance to P. falciparum infection in the Cellia subgenus, which comprises the most important malaria vectors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.