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Immune signaling pathways regulating bacterial and malaria parasite infection of the mosquito Anopheles gambiae
- Meister, S., Kanzok, S.M., Zheng, X.I., Luna, C., Li, T.R., Hoa, N.T., Clayton, J.R., White, K.P., Kafatos, F.C., Christophides, G.K.
- Proceedings of the National Academy of Sciences of the United States of America 2005 v.102 no.32 pp. 11420-11425
- Anopheles gambiae, disease vectors, insect vectors, Plasmodium berghei, infection, bacterial infections, Staphylococcus aureus, Escherichia coli, disease resistance, immune response, antimicrobial peptides, gene expression regulation, transcription factors, messenger RNA, microarray technology
- We show that, in the malaria vector Anopheles gambiae, expression of Cecropin 1 is regulated by REL2, an NF-kappaB-like transcription factor orthologous to Drosophila Relish. Through alternative splicing, REL2 produces a full-length (REL2-F) and a shorter (REL2-S) protein isoform lacking the inhibitory ankyrin repeats and death domain. RNA interference experiments show that, in contrast to Drosophila Relish, which responds solely to Gram-negative bacteria, the Anopheles REL2-F and REL2-S isoforms are involved in defense against the Gram-positive Staphylococcus aureus and the Gram-negative Escherichia coli bacteria, respectively. REL2-F also regulates the intensity of mosquito infection with the malaria parasite, Plasmodium berghei. The adaptor IMD shares the same activities as REL2-F. Microarray analysis identified 10 additional genes regulated by REL2, including CEC3, GAM1, and LRIM1.