20S proteasomes secreted by the malaria parasite promote its growth.
Biological Transport
/ physiology
Cytoskeleton
/ metabolism
Erythrocytes
/ cytology
Host-Parasite Interactions
/ physiology
Humans
Malaria, Falciparum
/ metabolism
Membrane Proteins
/ metabolism
Phosphorylation
Plasmodium falciparum
/ growth & development
Proteasome Endopeptidase Complex
/ metabolism
Proteomics
Journal
Nature communications
ISSN: 2041-1723
Titre abrégé: Nat Commun
Pays: England
ID NLM: 101528555
Informations de publication
Date de publication:
19 02 2021
19 02 2021
Historique:
received:
14
09
2020
accepted:
20
01
2021
entrez:
20
2
2021
pubmed:
21
2
2021
medline:
12
3
2021
Statut:
epublish
Résumé
Mature red blood cells (RBCs) lack internal organelles and canonical defense mechanisms, making them both a fascinating host cell, in general, and an intriguing choice for the deadly malaria parasite Plasmodium falciparum (Pf), in particular. Pf, while growing inside its natural host, the human RBC, secretes multipurpose extracellular vesicles (EVs), yet their influence on this essential host cell remains unknown. Here we demonstrate that Pf parasites, cultured in fresh human donor blood, secrete within such EVs assembled and functional 20S proteasome complexes (EV-20S). The EV-20S proteasomes modulate the mechanical properties of naïve human RBCs by remodeling their cytoskeletal network. Furthermore, we identify four degradation targets of the secreted 20S proteasome, the phosphorylated cytoskeletal proteins β-adducin, ankyrin-1, dematin and Epb4.1. Overall, our findings reveal a previously unknown 20S proteasome secretion mechanism employed by the human malaria parasite, which primes RBCs for parasite invasion by altering membrane stiffness, to facilitate malaria parasite growth.
Identifiants
pubmed: 33608523
doi: 10.1038/s41467-021-21344-8
pii: 10.1038/s41467-021-21344-8
pmc: PMC7895969
doi:
Substances chimiques
Membrane Proteins
0
Proteasome Endopeptidase Complex
EC 3.4.25.1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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