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Plasmodium UIS3 sequesters host LC3 to avoid elimination by autophagy in hepatocytes
Eliana Real1, Lénia Rodrigues1, Ghislain G Cabal1
1Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.
Nature Microbiology
|November 8, 2017
Summary
Malaria parasites use the UIS3 protein to evade host cell autophagy. UIS3 binds to LC3, blocking the autophagy process and preventing parasite elimination, offering a potential drug target.
Area of Science:
- Cell Biology
- Parasitology
- Immunology
Background:
- Malaria parasites (Plasmodium) reside within a parasitophorous vacuole (PV) during host cell infection.
- Autophagy is a cellular process that targets intracellular pathogens for degradation.
- Plasmodium parasites face autophagy as a threat, with the PV membrane (PVM) marked by autophagy proteins like LC3.
Purpose of the Study:
- To investigate how Plasmodium parasites evade host cell autophagy.
- To identify the role of the PVM protein UIS3 in autophagy evasion.
- To explore the UIS3-LC3 interaction as a potential therapeutic target.
Main Methods:
- Investigated Plasmodium berghei infection in hepatic cells.
- Analyzed the interaction between UIS3 and host cell LC3.
- Characterized UIS3's function in inhibiting autophagy.
Main Results:
- Plasmodium berghei utilizes the PVM protein UIS3 to evade host-cell-mediated autophagy.
- UIS3 binds to host LC3 via a non-canonical interaction site.
- UIS3 competitively inhibits LC3 binding by host proteins, acting as an autophagy inhibitor.
Conclusions:
- UIS3 is a key mediator of autophagy evasion in Plasmodium parasites.
- The UIS3-LC3 interaction is a novel mechanism for pathogen survival.
- Targeting the UIS3-LC3 interaction could lead to new antimalarial drug development.
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