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Active APPL1 sequestration by Plasmodium favors liver-stage development.

Aparajita Lahree1, Sara de Jesus Santos Baptista2, Sofia Marques2

  • 1Instituto de Medicina Molecular- João Lobo Antunes (iMM-JLA), Faculdade de Medicina, Universidade de Lisboa, Av. Prof. Egas Moniz, 1649-028 Lisboa, Portugal; Departamento de Bioengenharia, Instituto Superior Técnico, Av. Rovisco Pais 1, 1049-001 Lisboa, Portugal.

Cell Reports
|June 1, 2022
PubMed
Summary

Plasmodium parasites sequester host APPL1 protein at the parasitophorous vacuole membrane (PVM), involving Plasmodium Rab5b. This interaction impacts parasite size during liver-stage development.

Keywords:
APPL1CP: MicrobiologyPbRab5bPlasmodiumendosomehepatocytesliver-stagemalaria

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Area of Science:

  • Cellular microbiology
  • Parasitology
  • Host-pathogen interactions

Background:

  • Intracellular pathogens manipulate host cellular processes for survival.
  • Endocytosis signaling pathways are crucial host machineries targeted during infection.

Purpose of the Study:

  • To investigate the role of host endosomal-adaptor protein APPL1 in Plasmodium liver-stage infection.
  • To elucidate the mechanism by which Plasmodium parasites interact with host endosomal pathways.

Main Methods:

  • Investigated the interaction between Plasmodium parasites and host APPL1.
  • Utilized Plasmodium Rab5b and host Rab5 mutants (hRab5_Q79L, PbRab5b_Q91L) to study PVM protein localization and parasite development.
  • Assessed parasite size and APPL1 enrichment at the PVM.

Main Results:

  • Plasmodium parasites sequester host APPL1 at the parasitophorous vacuole membrane (PVM).
  • This sequestration involves an atypical Plasmodium Rab5 isoform (Rab5b).
  • Overexpression of a GTPase-deficient host Rab5 mutant (hRab5_Q79L) resulted in smaller parasites and reduced PVM APPL1.
  • A GTPase-deficient Plasmodium berghei Rab5b mutant (PbRab5b_Q91L) rescued PVM APPL1 signal and parasite size.

Conclusions:

  • A strong correlation exists between APPL1 retention at the PVM and parasite size during exoerythrocytic development.
  • Plasmodium parasites actively manipulate host endosomal trafficking machinery, specifically involving APPL1 and Rab5b, to regulate their development.