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Co-option of Plasmodium falciparum PP1 for egress from host erythrocytes

Author

Listed:
  • Aditya S. Paul

    (Harvard T. H. Chan School of Public Health)

  • Alexandra Miliu

    (Université de Montpellier)

  • Joao A. Paulo

    (Harvard Medical School)

  • Jonathan M. Goldberg

    (Harvard T. H. Chan School of Public Health)

  • Arianna M. Bonilla

    (Harvard T. H. Chan School of Public Health)

  • Laurence Berry

    (Université de Montpellier)

  • Marie Seveno

    (Université de Montpellier)

  • Catherine Braun-Breton

    (Université de Montpellier)

  • Aziz L. Kosber

    (Harvard T. H. Chan School of Public Health)

  • Brendan Elsworth

    (Harvard T. H. Chan School of Public Health)

  • Jose S. N. Arriola

    (Harvard T. H. Chan School of Public Health)

  • Maryse Lebrun

    (Université de Montpellier)

  • Steven P. Gygi

    (Harvard Medical School)

  • Mauld H. Lamarque

    (Université de Montpellier)

  • Manoj T. Duraisingh

    (Harvard T. H. Chan School of Public Health)

Abstract

Asexual proliferation of the Plasmodium parasites that cause malaria follows a developmental program that alternates non-canonical intraerythrocytic replication with dissemination to new host cells. We carried out a functional analysis of the Plasmodium falciparum homolog of Protein Phosphatase 1 (PfPP1), a universally conserved cell cycle factor in eukaryotes, to investigate regulation of parasite proliferation. PfPP1 is indeed required for efficient replication, but is absolutely essential for egress of parasites from host red blood cells. By phosphoproteomic and chemical-genetic analysis, we isolate two functional targets of PfPP1 for egress: a HECT E3 protein-ubiquitin ligase; and GCα, a fusion protein composed of a guanylyl cyclase and a phospholipid transporter domain. We hypothesize that PfPP1 regulates lipid sensing by GCα and find that phosphatidylcholine stimulates PfPP1-dependent egress. PfPP1 acts as a key regulator that integrates multiple cell-intrinsic pathways with external signals to direct parasite egress from host cells.

Suggested Citation

  • Aditya S. Paul & Alexandra Miliu & Joao A. Paulo & Jonathan M. Goldberg & Arianna M. Bonilla & Laurence Berry & Marie Seveno & Catherine Braun-Breton & Aziz L. Kosber & Brendan Elsworth & Jose S. N. A, 2020. "Co-option of Plasmodium falciparum PP1 for egress from host erythrocytes," Nature Communications, Nature, vol. 11(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-17306-1
    DOI: 10.1038/s41467-020-17306-1
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    Cited by:

    1. Kieran Tebben & Salif Yirampo & Drissa Coulibaly & Abdoulaye K. Koné & Matthew B. Laurens & Emily M. Stucke & Ahmadou Dembélé & Youssouf Tolo & Karim Traoré & Amadou Niangaly & Andrea A. Berry & Boure, 2024. "Gene expression analyses reveal differences in children’s response to malaria according to their age," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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