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Fig. 11 | Parasites & Vectors

Fig. 11

From: Abscisic acid induces a transient shift in signaling that enhances NF-κB-mediated parasite killing in the midgut of Anopheles stephensi without reducing lifespan or fecundity

Fig. 11

Model of ABA signaling within the mosquito midgut upon ingestion of a P. falciparum-infected bloodmeal. Within minutes of feeding, ABA increases TAK1 and GSK3 activity levels within the midgut. Active GSK3 reduces phosphorylation and activity of AMPK. TAK1 signaling increases NF-κB activity and downstream immune gene expression (apl1, nos, tep1), which is enhanced by the changes in GSK3 and AMPK levels. NOS catalyzes the synthesis of NO which kills parasites and transiently damages the midgut, as evidenced by decreased cellular replication and differentiation (pros/esg) and autophagy (atg6/8). However, these changes are temporally limited and ultimately have no effect on lifespan. Reduced levels of ilp3 and ilp4 are conducive to increased nos expression and reduced infection, but are short-lived and have no effect on fecundity

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