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Malaria starts with the infection of the liver of the host by  Plasmodium  sporozoites, the parasite form transmitted by infected mosquitoes. Sporozoites migrate through several hepatocytes by breaching their plasma membranes before finally infecting one with the formation of an internalization vacuole. Migration through host cells induces apical regulated exocytosis in sporozoites. Here we show that apical regulated exocytosis is induced by increases in cAMP in sporozoites of rodent ( P. yoelii  and  P. berghei ) and human ( P. falciparum )  Plasmodium  species. We have generated  P. berghei  parasites deficient in adenylyl cyclase α ( AC α), a gene containing regions with high homology to adenylyl cyclases.  PbAC α-deficient sporozoites do not exocytose in response to migration through host cells and present more than 50% impaired hepatocyte infectivity  in vivo . These effects are specific to  AC α, as re-introduction of  AC α in deficient parasites resulted in complete recovery of exocytosis and infection. Our findings indicate that  AC α and increases in cAMP levels are required for sporozoite apical regulated exocytosis, which is involved in sporozoite infection of hepatocytes.

Adenylyl Cyclase α and cAMP Signaling Mediate Plasmodium Sporozoite Apical Regulated Exocytosis and Hepatocyte Infection