An obligatory step in the complex life cycle of the
malaria parasite is sporogony, which occurs during the oocyst stage in adult female Anopheles mosquitoes. Sporogony is metabolically demanding, and successful oocyst maturation is dependent on host
lipids. In insects,
lipid energy reserves are mobilized by adipokinetic
hormones (AKHs). We hypothesized that Plasmodium falciparum
infection activates Anopheles gambiae AKH signaling and lipid mobilization. We profiled the expression patterns of AKH pathway genes and AgAkh1
peptide levels in An. gambiae during
starvation, after blood feeding, and following
infection and observed a significant time-dependent up-regulation of AKH pathway genes and
peptide levels during
infection. Depletion of AgAkh1 and AgAkhR by RNAi reduced salivary gland sporozoite production, while synthetic AgAkh1
peptide supplementation rescued sporozoite numbers. Inoculation of uninfected female mosquitoes with supernatant from P. falciparum-infected midguts activated AKH signaling. Clearly, identifying the parasite molecules mediating AKH signaling in P. falciparum sporogony is paramount.