Publications des scientifiques de l'IRD

Nsango S. E., Pompon J., Xie T., Rademacher A., Fraiture M., Thoma M., Awono-Ambene P. H., Moyou R. S., Morlais Isabelle, Levashina E. A. (2013). AP-1/Fos-TGase2 axis mediates wounding-induced Plasmodium falciparum killing in Anopheles gambiae. Journal of Biological Chemistry, 288 (22), p. 16145-16154. ISSN 0021-9258.

Titre du document
AP-1/Fos-TGase2 axis mediates wounding-induced Plasmodium falciparum killing in Anopheles gambiae
Année de publication
2013
Type de document
Article référencé dans le Web of Science WOS:000319822300065
Auteurs
Nsango S. E., Pompon J., Xie T., Rademacher A., Fraiture M., Thoma M., Awono-Ambene P. H., Moyou R. S., Morlais Isabelle, Levashina E. A.
Source
Journal of Biological Chemistry, 2013, 288 (22), p. 16145-16154 ISSN 0021-9258
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.
Plan de classement
Sciences fondamentales / Techniques d'analyse et de recherche [020] ; Entomologie médicale / Parasitologie / Virologie [052]
Identifiant IRD
PAR00010610
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