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

Abstract 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...

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Autores principales: Anna Moskovskich, Ulrich Goldmann, Felix Kartnig, Sabrina Lindinger, Justyna Konecka, Giuseppe Fiume, Enrico Girardi, Giulio Superti-Furga
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Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/944d2ce2c8604b0bbe43e2bca30a71f0
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spelling oai:doaj.org-article:944d2ce2c8604b0bbe43e2bca30a71f02021-12-02T15:07:53ZThe transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection10.1038/s41598-019-46952-92045-2322https://doaj.org/article/944d2ce2c8604b0bbe43e2bca30a71f02019-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-46952-9https://doaj.org/toc/2045-2322Abstract 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.Anna MoskovskichUlrich GoldmannFelix KartnigSabrina LindingerJustyna KoneckaGiuseppe FiumeEnrico GirardiGiulio Superti-FurgaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-11 (2019)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Anna Moskovskich
Ulrich Goldmann
Felix Kartnig
Sabrina Lindinger
Justyna Konecka
Giuseppe Fiume
Enrico Girardi
Giulio Superti-Furga
The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
description Abstract 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.
format article
author Anna Moskovskich
Ulrich Goldmann
Felix Kartnig
Sabrina Lindinger
Justyna Konecka
Giuseppe Fiume
Enrico Girardi
Giulio Superti-Furga
author_facet Anna Moskovskich
Ulrich Goldmann
Felix Kartnig
Sabrina Lindinger
Justyna Konecka
Giuseppe Fiume
Enrico Girardi
Giulio Superti-Furga
author_sort Anna Moskovskich
title The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
title_short The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
title_full The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
title_fullStr The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
title_full_unstemmed The transporters SLC35A1 and SLC30A1 play opposite roles in cell survival upon VSV virus infection
title_sort transporters slc35a1 and slc30a1 play opposite roles in cell survival upon vsv virus infection
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/944d2ce2c8604b0bbe43e2bca30a71f0
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