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The innate immune system of  Anopheles gambiae  mosquitoes limits  Plasmodium  infection through multiple molecular mechanisms. For example, midgut invasion by the parasite triggers an epithelial nitration response that promotes activation of the complement-like system. We found that suppression of the JNK pathway, by silencing either  Hep ,  JNK ,  Jun  or  Fos  expression, greatly enhanced  Plasmodium  infection; while overactivating this cascade, by silencing the suppressor  Puckered , had the opposite effect. The JNK pathway limits infection via two coordinated responses. It induces the expression of two enzymes (HPx2 and NOX5) that potentiate midgut epithelial nitration in response to  Plasmodium  infection and regulates expression of two key hemocyte-derived immune effectors (TEP1 and FBN9). Furthermore, the  An. gambiae  L3–5 strain that has been genetically selected to be refractory (R) to  Plasmodium  infection exhibits constitutive overexpression of genes from the JNK pathway, as well as midgut and hemocyte effector genes. Silencing experiments confirmed that this cascade mediates, to a large extent, the drastic parasite elimination phenotype characteristic of this mosquito strain. In sum, these studies revealed the JNK pathway as a key regulator of the ability of  An. gambiae  mosquitoes to limit  Plasmodium  infection and identified several effector genes mediating these responses.

The JNK Pathway Is a Key Mediator of Anopheles gambiae Antiplasmodial Immunity