Deletion of the Plasmodium falciparum exported protein PTP7 leads to Maurer&#39;s clefts vesiculation, host cell remodeling defects, and loss of surface presentation of EMP1

Carmo, OMS; Shami, GJ; Cox, D; Liu, B; Blanch, AJ; Tiash, S; Tilley, L; Dixon, MWA

Deletion of the Plasmodium falciparum exported protein PTP7 leads to Maurer's clefts vesiculation, host cell remodeling defects, and loss of surface presentation of EMP1

Author(s): Carmo, OMS; Shami, GJ; Cox, D; Liu, B; Blanch, AJ; Tiash, S; Tilley, L; Dixon, MWA;
Details: Publication Year 2022-08-05,Volume 18,Issue #8,Page e1009882
Journal Title: PLOS Pathogens
Abstract: Presentation of the variant antigen, Plasmodium falciparum erythrocyte membrane protein 1 (EMP1), at knob-like protrusions on the surface of infected red blood cells, underpins the parasite's pathogenicity. Here we describe a protein PF3D7_0301700 (PTP7), that functions at the nexus between the intermediate trafficking organelle, the Maurer's cleft, and the infected red blood cell surface. Genetic disruption of PTP7 leads to accumulation of vesicles at the Maurer's clefts, grossly aberrant knob morphology, and failure to deliver EMP1 to the red blood cell surface. We show that an expanded low complexity sequence in the C-terminal region of PTP7, identified only in the Laverania clade of Plasmodium, is critical for efficient virulence protein trafficking.
Publisher: PLOS
Research Division(s): Infectious Diseases And Immune Defence
PubMed ID: 35930605
Publisher's Version: https://doi.org/10.1371/journal.ppat.1009882
Open Access at Publisher's Site: https://doi.org/10.1371/journal.ppat.100988
NHMRC Grants: NHMRC/1098992,
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 2022-08-08 09:15:45

Last Modified: 2022-08-25 08:51:04