Latest article (May 2013)

AP-1/Fos-TGase2 axis mediates wounding-induced Plasmodium falciparum killing in Anopheles gambiaeNsango SE, Pompon J, Xie T, Rademacher A, Fraiture M, Thoma M, Awono-Ambene PH, Moyou RS, Morlais I, Levashina EA., 2013 – J Biol Chem. [Epub ahead of print] pubmed

Abstract

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 P. 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 A. gambiae.