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Cyclic AMP signalling controls key components of malaria parasite host cell invasion machinery

Avnish Patel1, Abigail J Perrin2, Helen R Flynn3

  • 1Faculty of Infectious Diseases, London School of Hygiene & Tropical Medicine, London, United Kingdom.

Plos Biology
|May 11, 2019
PubMed

Insights

Cyclic AMP (cAMP) and protein kinase A (PKA) are vital for malaria parasite Plasmodium falciparum to invade red blood cells. However, parasite development proceeds without this signaling pathway, which also impacts key invasion proteins like AMA1.

Area of Science:

  • Molecular parasitology
  • Cellular signaling pathways
  • Malaria pathogenesis

Background:

  • The role of cyclic adenosine monophosphate (cAMP) in malaria parasite Plasmodium falciparum blood stage development remains largely uncharacterized.
  • cAMP is a crucial signaling molecule with diverse functions across evolutionary species.
  • Understanding cAMP's function in P. falciparum is essential for developing novel antimalarial strategies.

Purpose of the Study:

  • To investigate the role of cAMP and its downstream effector, cAMP-dependent protein kinase (PKA), in the asexual blood stage development of P. falciparum.
  • To determine the necessity of cAMP-dependent signaling for erythrocyte invasion and other developmental stages.
  • To explore the function of Plasmodium falciparum EPAC (PfEpac) in blood stages and identify cAMP-dependent phosphorylation targets.

Main Methods:

  • Conditional disruption of adenylyl cyclase beta (ACβ) to inhibit cAMP production.
  • Assessment of cAMP-dependent protein kinase (PKA) activity.
  • Analysis of parasite development and erythrocyte invasion efficiency.
  • Phosphoproteomic analysis to identify cAMP-dependent phosphorylation sites.

Main Results:

  • Both cAMP production and PKA activity are essential for Plasmodium falciparum erythrocyte invasion.
  • Key developmental stages preceding invasion occur independently of cAMP-dependent signaling.
  • Plasmodium falciparum EPAC (PfEpac) is not essential for blood stage development.
  • Numerous phosphorylation sites dependent on cAMP signaling were identified, including on the apical membrane antigen 1 (AMA1) invasion adhesin.

Conclusions:

  • cAMP-dependent signaling, primarily through PKA, is critical for the final invasion step of Plasmodium falciparum into erythrocytes.
  • While essential for invasion, cAMP signaling is not required for earlier developmental transitions.
  • Phosphorylation of AMA1 by cAMP-dependent pathways regulates erythrocyte invasion, offering a potential target for antimalarial drugs.

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