Shedding of host autophagic proteins from the parasitophorous vacuolar membrane of Plasmodium berghei

The hepatic stage of the malaria parasite Plasmodium is accompanied by an autophagy-mediated host response directly targeting the parasitophorous vacuolar membrane (PVM) harbouring the parasite. Removal of the PVM-associated autophagic proteins such as ubiquitin, p62, and LC3 correlates with parasit...

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Bibliographic Details
Published in:Scientific reports 2017-05, Vol.7 (1), p.2191-14, Article 2191
Main Authors: Agop-Nersesian, Carolina, De Niz, Mariana, Niklaus, Livia, Prado, Monica, Eickel, Nina, Heussler, Volker T.
Format: Article
Language:English
Subjects:
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Animals
Autophagy
Cell Line
Cytoplasm
Cytoplasm - metabolism
Genes, Reporter
Host-Parasite Interactions
Humanities and Social Sciences
Humans
Immune system
Liver - metabolism
Liver - parasitology
Malaria
Malaria - metabolism
Malaria - parasitology
Mice
Mice, Transgenic
Microtubule-Associated Proteins - genetics
Microtubule-Associated Proteins - metabolism
Models, Biological
multidisciplinary
Parasites
Phagocytosis
Plasmodium
Plasmodium berghei - physiology
Protein Transport
Science
Science (multidisciplinary)
Time-Lapse Imaging
Ubiquitin
Vacuoles - metabolism
Vector-borne diseases
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Summary:The hepatic stage of the malaria parasite Plasmodium is accompanied by an autophagy-mediated host response directly targeting the parasitophorous vacuolar membrane (PVM) harbouring the parasite. Removal of the PVM-associated autophagic proteins such as ubiquitin, p62, and LC3 correlates with parasite survival. Yet, it is unclear how Plasmodium avoids the deleterious effects of selective autophagy. Here we show that parasites trap host autophagic factors in the tubovesicular network (TVN), an expansion of the PVM into the host cytoplasm. In proliferating parasites, PVM-associated LC3 becomes immediately redirected into the TVN, where it accumulates distally from the parasite’s replicative centre. Finally, the host factors are shed as vesicles into the host cytoplasm. This strategy may enable the parasite to balance the benefits of the enhanced host catabolic activity with the risk of being eliminated by the cell’s cytosolic immune defence.
ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-017-02156-7