The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
18 07 2019
Historique:
received: 29 01 2019
accepted: 04 07 2019
entrez: 20 7 2019
pubmed: 20 7 2019
medline: 27 10 2020
Statut: epublish

Résumé

Host factor requirements for different classes of viruses have not been fully unraveled. Replication of the viral genome and synthesis of viral proteins within the human host cell are associated with an increased demand for nutrients and specific metabolites. With more than 400 acknowledged members to date in humans, solute carriers (SLCs) represent the largest family of transmembrane proteins dedicated to the transport of ions and small molecules such as amino acids, sugars and nucleotides. Consistent with their impact on cellular metabolism, several SLCs have been implicated as host factors affecting the viral life cycle and the cellular response to infection. In this study, we aimed at characterizing the role of host SLCs in cell survival upon viral infection by performing unbiased genetic screens using a focused CRISPR knockout library. Genetic screens with the cytolytic vesicular stomatitis virus (VSV) showed that the loss of two SLCs genes, encoding the sialic acid transporter SLC35A1/CST and the zinc transporter SLC30A1/ZnT1, affected cell survival upon infection. Further characterization of these genes suggests a role for both of these transporters in the apoptotic response induced by VSV, offering new insights into the cellular response to oncolytic virus infections.

Identifiants

pubmed: 31320712
doi: 10.1038/s41598-019-46952-9
pii: 10.1038/s41598-019-46952-9
pmc: PMC6639343
doi:

Substances chimiques

Cation Transport Proteins 0
Nucleotide Transport Proteins 0
SLC30A1 protein, human 0
SLC35A1 protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

10471

Subventions

Organisme : Austrian Science Fund FWF
ID : P 29250
Pays : Austria

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Auteurs

Anna Moskovskich (A)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Ulrich Goldmann (U)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Felix Kartnig (F)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Sabrina Lindinger (S)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Justyna Konecka (J)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Giuseppe Fiume (G)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria.

Enrico Girardi (E)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria. egirardi@cemm.oeaw.ac.at.

Giulio Superti-Furga (G)

CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090, Vienna, Austria. gsuperti@cemm.oeaw.ac.at.
Center for Physiology and Pharmacology, Medical University of Vienna, 1090, Vienna, Austria. gsuperti@cemm.oeaw.ac.at.

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Classifications MeSH