期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 288, 期 22, 页码 16145-16154出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M112.443267
关键词
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资金
- CNRS [UPR 9022]
- INSERM [U963]
- l'Institut de Recherche pour le Developpement (IRD)
- EC [223601, 242095]
- IRD-CNRS [6774.00]
- Fondation pour la Recherche Medicale (FRM)
- DSFIRD scholarship
- BIOMALPAR Ph.D. fellowship
Anopheline mosquitoes are the only vectors of human malaria worldwide. It is now widely accepted that mosquito immune responses play a crucial role in restricting Plasmodium development within the vector; therefore, further dissection of the molecular mechanisms underlying these processes should inform new vector control strategies urgently needed to roll back the disease. Here, using genome-wide transcriptional profiling, bioinformatics, and functional gene analysis, we identify a new axis of mosquito resistance to monoclonal Plasmodium falciparum infections that includes the AP-1 transcription factor Fos and the transglutaminase 2 (TGase2), a cross-linking enzyme with known roles in wound responses. We demonstrate that Fos regulates induction of TGase2 expression after wounding but does not affect expression of the components of the well characterized complement-like system. Silencing of Fos or of TGase2 aborts the wounding-induced mosquito killing of P. falciparum. These results reveal multiple signaling pathways that are required for efficient Plasmodium killing in Anopheles gambiae.
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