Abstract
We recently found that JAK/STAT signaling in skeletal muscles is important for the immune response of Drosophila larvae against wasp infection, but it was not clear how muscles could affect the immune response. Here we show that insulin signaling is required in muscles, but not in fat body or hemocytes, during larval development for an efficient encapsulation response and for the formation of lamellocytes. This effect requires TOR signaling. We show that muscle tissue affects the immune response by acting as a master regulator of carbohydrate metabolism in the infected animal, via JAK/STAT and insulin signaling in the muscles, and that there is indirect positive feedback between JAK/STAT and insulin signaling in the muscles. Specifically, stimulation of JAK/STAT signaling in the muscles can rescue the deficient immune response when insulin signaling is suppressed. Our results shed new light on the interaction between metabolism, immunity, and tissue communication.
Highlights
We recently found that JAK/STAT signaling in skeletal muscles is important for the immune response of Drosophila larvae against wasp infection, but it was not clear how muscles could affect the immune response
We show that muscle tissue affects the immune response by acting as a master regulator of carbohydrate metabolism in the infected animal, via JAK/STAT and insulin signaling in the muscles, and that there is indirect positive feedback between JAK/STAT and insulin signaling in the muscles
Our results suggest that JAK/STAT signaling in the muscles has profound effects on insulin signaling in the entire organism, that insulin in turn gives positive feedback on the JAK/STAT response, and that Drosophila larval skeletal muscles have a surprising role in the cellular immune response against wasp infection by controlling carbohydrate metabolism and feeding behavior
Summary
We recently found that JAK/STAT signaling in skeletal muscles is important for the immune response of Drosophila larvae against wasp infection, but it was not clear how muscles could affect the immune response. We show that insulin signaling is required in muscles, but not in fat body or hemocytes, during larval development for an efficient encapsulation response and for the formation of lamellocytes. Bacteria and fungi induce a humoral immune response, in which antimicrobial peptides are induced via Toll or Imd signaling[1,2,3,4] Larger pathogens, such as eggs laid by the parasitoid wasp Leptopilina boulardi, activate a cellular immune response[5,6,7] that involves three hemocyte classes: plasmatocytes, crystal cells, and lamellocytes. Besides the classical insulin pathway, Drosophila has two homologs to the relaxin receptor, Lgr[3] and Lgr[4], of which at least Lgr[3] can serve as a receptor for the insulin-like peptide Ilp[831–33]
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