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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.