Innexin AGAP001476 Is Critical for Mediating Anti-Plasmodium Responses in Anopheles Mosquitoes

摘要: The Toll and IMD pathways are known to be induced upon Plasmodium berghei falciparum infection, respectively. It is unclear how or other pathogens in the blood meal their invasion of midgut epithelium would trigger innate immune responses cells, particular hemocytes. Gap junctions, which can mediate both cell-to-cell cell-to-extracellular communication, may participate this signal transduction. This study examined whether innexins, gap junction proteins insects, involved anti-Plasmodium Anopheles gambiae. Inhibitor studies using carbenoxolone indicated that blocking innexons resulted an increase oocyst number infection prevalence. was accompanied by a decline TEP1 levels carbenoxolone-treated mosquitoes. Innexin AGAP001476 mRNA midguts were during knockdown AGAP001476, but not AGAP006241, caused induction number. Silencing concurrent vitellogenin levels, inhibitor, addition reduced level TEP1-LRIM1-APL1C complex hemolymph. Both regulated Cactus under pathway. Simultaneous cactus failed reverse near refractoriness cactus, suggesting AGAP001476-mediated response Cactus-dependent. These data demonstrate critical role for innexin mediating against through pathway