Journal Article

DZNE-2020-06129

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Prion strains depend on different endocytic routes for productive infection.

Fehlinger, A. (First author)DZNE* ; Wolf, H.DZNE* ; Hossinger, A.DZNE* ; Dürnberger, Y.DZNE* ; Pleschka, C.DZNE* ; Riemschoß, K.DZNE* ; Liu, S.DZNE* ; Bester, R. ; Paulsen, L.DZNE* ; Priola, S. A. ; Groschup, M. H. ; Schätzl, H. M. ; Vorberg, I. M. (Last author)DZNE*

2017
Macmillan Publishers Limited, part of Springer Nature [London]

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Please use a persistent id in citations: doi:10.1038/s41598-017-07260-2

Abstract: Prions are unconventional agents composed of misfolded prion protein that cause fatal neurodegenerative diseases in mammals. Prion strains induce specific neuropathological changes in selected brain areas. The mechanism of strain-specific cell tropism is unknown. We hypothesised that prion strains rely on different endocytic routes to invade and replicate within their target cells. Using prion permissive cells, we determined how impairment of endocytosis affects productive infection by prion strains 22L and RML. We demonstrate that early and late stages of prion infection are differentially sensitive to perturbation of clathrin- and caveolin-mediated endocytosis. Manipulation of canonical endocytic pathways only slightly influenced prion uptake. However, blocking the same routes had drastic strain-specific consequences on the establishment of infection. Our data argue that prion strains use different endocytic pathways for infection and suggest that cell type-dependent differences in prion uptake could contribute to host cell tropism.

Keyword(s): Animals (MeSH) ; Biological Transport (MeSH) ; Caveolin 1: metabolism (MeSH) ; Cell Line (MeSH) ; Cell Membrane: metabolism (MeSH) ; Endocytosis (MeSH) ; Mice (MeSH) ; PrPSc Proteins: metabolism (MeSH) ; PrPSc Proteins: pathogenicity (MeSH) ; Prion Diseases: metabolism (MeSH) ; Cav1 protein, mouse ; Caveolin 1 ; PrPSc Proteins

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Contributing Institute(s):

1. Prion Cell Biology (AG Vorberg)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2017

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