ArticleProceedings of the National Academy of Sciences of the United States of America2015
Plasmodium falciparum evades mosquito immunity by disrupting JNK-mediated apoptosis of invaded midgut cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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Who cites it
83 citing papers in PubMed, 126 citations in OpenAlex.
- Malaria mosquito antimicrobial defence requires immunity and detoxification gene regulation by Lola.Insect molecular biology · 2026Article
- Single-cell insights: Mosquito Toll activation enhances granulocyte differentiation and immune surveillance via Notch suppression.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- From gatekeeper to target: MAPK cascades as control circuits at the insect-microbe interface.FEMS microbiology reviews · 2026Review
- Blood feeding, microbiota, and layered mosquito immunity: from pathway phenotypes to vector competence.Frontiers in immunology · 2026Review
- Advancing Malaria Vector Control: Insights Into Mosquito Immunity and Genetic Strategies.TheScientificWorldJournal · 2026Review
- Warmer temperature accelerates senescence by modifying the aging-dependent changes in the mosquito transcriptome, altering immunity, metabolism, and DNA repair.Immunity & ageing : I & A · 2025Article
- Avian malaria and the overlooked metabolic pathways underlying mosquitoRoyal Society open science · 2025Article
- Worldwide genetic diversity of Plasmodium vivax Pv47 is consistent with natural selection by anopheline mosquitoes.Nature communications · 2025Article
- TNF signaling mediates cellular immune function and promotes malaria parasite killing in the mosquito Anopheles gambiae.PLoS pathogens · 2025Article
- Mosquito immune responses to Plasmodium parasites that limit malaria transmission.Cellular and molecular life sciences : CMLS · 2025Review
- Plasmodium falciparum Pfs47 haplotype compatibility to Anopheles gambiae in Kisumu, a malaria-endemic region of Kenya.Scientific reports · 2025Article
- Anopheles gambiae phagocytic hemocytes promote Plasmodium falciparum infection by regulating midgut epithelial integrity.Nature communications · 2025Article
- Article
- Evolution and assembly ofOpen biology · 2023Article
- Mechanism of Immune Evasion in Mosquito-Borne Diseases.Pathogens (Basel, Switzerland) · 2023Review
- Immune gene expression in the mosquito vector Culex quinquefasciatus during an avian malaria infection.Molecular ecology · 2023Article
- Evidence of a conserved mammalian immunosuppression mechanism inFrontiers in immunology · 2023Article
- Deceiving and escaping complement - the evasive journey of the malaria parasite.Trends in parasitology · 2022Review
- The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host's Complement System.Biomolecules · 2022Review
- Pfs47 as a Malaria Transmission-Blocking Vaccine Target.The American journal of tropical medicine and hygiene · 2022Article
23 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The malaria parasite, Plasmodium, must survive and develop in the mosquito vector to be successfully transmitted to a new host. The Plasmodium falciparum Pfs47 gene is critical for malaria transmission. Parasites that express Pfs47 (NF54 WT) evade mosquito immunity and survive, whereas Pfs47 knockouts (KO) are efficiently eliminated by the complement-like system. Two alternative approaches were used to investigate the mechanism of action of Pfs47 on immune evasion. First, we examined whether Pfs47 affected signal transduction pathways mediating mosquito immune responses, and show that the Jun-N-terminal kinase (JNK) pathway is a key mediator of Anopheles gambiae antiplasmodial responses to P. falciparum infection and that Pfs47 disrupts JNK signaling. Second, we used microarrays to compare the global transcriptional responses of A. gambiae midguts to infection with WT and KO parasites. The presence of Pfs47 results in broad and profound changes in gene expression in response to infection that are already evident 12 h postfeeding, but become most prominent at 26 h postfeeding, the time when ookinetes invade the mosquito midgut. Silencing of 15 differentially expressed candidate genes identified caspase-S2 as a key effector of Plasmodium elimination in parasites lacking Pfs47. We provide experimental evidence that JNK pathway regulates activation of caspases in Plasmodium-invaded midgut cells, and that caspase activation is required to trigger midgut epithelial nitration. Pfs47 alters the cell death pathway of invaded midgut cells by disrupting JNK signaling and prevents the activation of several caspases, resulting in an ineffective nitration response that makes the parasite undetectable by the mosquito complement-like system.
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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 OpenQuestion graph.