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The Plasmodium translocon of exported proteins component EXP2 is critical for establishing a patent malaria infection in mice

Version 2 2024-06-04, 07:14
Version 1 2015-09-30, 16:50
journal contribution
posted on 2024-06-04, 07:14 authored by M Kalanon, D Bargieri, A Sturm, K Matthews, S Ghosh, CD Goodman, S Thiberge, V Mollard, GI Mcfadden, R Ménard, Tania De Koning-WardTania De Koning-Ward
Export of most malaria proteins into the erythrocyte cytosol requires the Plasmodium Translocon of Exported proteins (PTEX) and a cleavable Plasmodium Export Element (PEXEL). In contrast, the contribution of PTEX in the liver stages and export of liver stage proteins is unknown. Here, using the FLP/FRT conditional mutatagenesis system, we generate transgenic P. berghei parasites deficient in EXP2, the putative pore-forming component of PTEX. Our data reveal that EXP2 is important for parasite growth in the liver and critical for parasite transition to the blood, with parasites impaired in their ability to generate a patent blood-stage infection. Surprisingly, whilst parasites expressing a functional PTEX machinery can efficiently export a PEXEL-bearing GFP reporter into the erythrocyte cytosol during a blood stage infection, this same reporter aggregates in large accumulations within the confines of the parasitophorous vacuole membrane during hepatocyte growth. Notably HSP101, the putative molecular motor of PTEX, could not be detected during the early liver stages of infection, which may explain why direct protein translocation of this soluble PEXEL-bearing reporter or indeed native PEXEL proteins into the hepatocyte cytosol has not been observed. This suggests that PTEX function may not be conserved between the blood and liver stages of malaria infection. This article is protected by copyright. All rights reserved.

History

Journal

Cellular Microbiology

Volume

18

Pagination

399-412

Location

India

Open access

  • Yes

ISSN

1462-5814

eISSN

1462-5822

Language

English

Publication classification

C Journal article, C1 Refereed article in a scholarly journal

Copyright notice

2015, Wiley

Issue

3

Publisher

WILEY