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Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes
Reconstituted Sendai viral envelopes (virosomes) are well recognized for their promising potential in membrane fusion–mediated delivery of bioactive molecules to liver cells. Despite the known function of viral envelope glycoproteins in catalyzing fusion with cellular membrane, the role of host cell...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The American Society for Cell Biology
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739296/ https://www.ncbi.nlm.nih.gov/pubmed/29074568 http://dx.doi.org/10.1091/mbc.E17-06-0400 |
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author | Chandra, Sunandini Kalaivani, Raju Kumar, Manoj Srinivasan, Narayanaswamy Sarkar, Debi P. |
author_facet | Chandra, Sunandini Kalaivani, Raju Kumar, Manoj Srinivasan, Narayanaswamy Sarkar, Debi P. |
author_sort | Chandra, Sunandini |
collection | PubMed |
description | Reconstituted Sendai viral envelopes (virosomes) are well recognized for their promising potential in membrane fusion–mediated delivery of bioactive molecules to liver cells. Despite the known function of viral envelope glycoproteins in catalyzing fusion with cellular membrane, the role of host cell proteins remains elusive. Here, we used two-dimensional differential in-gel electrophoresis to analyze hepatic cells in early response to virosome-induced membrane fusion. Quantitative mass spectrometry together with biochemical analysis revealed that villin, an actin-modifying protein, is differentially up-regulated and phosphorylated at threonine 206—an early molecular event during membrane fusion. We found that villin influences actin dynamics and that this influence, in turn, promotes membrane mixing through active participation of Sendai viral envelope glycoproteins. Modulation of villin in host cells also resulted in a discernible effect on the entry and egress of progeny Sendai virus. Taken together, these results suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor villin. |
format | Online Article Text |
id | pubmed-5739296 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The American Society for Cell Biology |
record_format | MEDLINE/PubMed |
spelling | pubmed-57392962018-03-02 Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes Chandra, Sunandini Kalaivani, Raju Kumar, Manoj Srinivasan, Narayanaswamy Sarkar, Debi P. Mol Biol Cell Articles Reconstituted Sendai viral envelopes (virosomes) are well recognized for their promising potential in membrane fusion–mediated delivery of bioactive molecules to liver cells. Despite the known function of viral envelope glycoproteins in catalyzing fusion with cellular membrane, the role of host cell proteins remains elusive. Here, we used two-dimensional differential in-gel electrophoresis to analyze hepatic cells in early response to virosome-induced membrane fusion. Quantitative mass spectrometry together with biochemical analysis revealed that villin, an actin-modifying protein, is differentially up-regulated and phosphorylated at threonine 206—an early molecular event during membrane fusion. We found that villin influences actin dynamics and that this influence, in turn, promotes membrane mixing through active participation of Sendai viral envelope glycoproteins. Modulation of villin in host cells also resulted in a discernible effect on the entry and egress of progeny Sendai virus. Taken together, these results suggest a novel mechanism of regulated viral entry in animal cells mediated by host factor villin. The American Society for Cell Biology 2017-12-15 /pmc/articles/PMC5739296/ /pubmed/29074568 http://dx.doi.org/10.1091/mbc.E17-06-0400 Text en © 2017 Chandra et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0). “ASCB®,” “The American Society for Cell Biology®,” and “Molecular Biology of the Cell®” are registered trademarks of The American Society for Cell Biology. |
spellingShingle | Articles Chandra, Sunandini Kalaivani, Raju Kumar, Manoj Srinivasan, Narayanaswamy Sarkar, Debi P. Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title | Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title_full | Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title_fullStr | Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title_full_unstemmed | Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title_short | Sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
title_sort | sendai virus recruits cellular villin to remodel actin cytoskeleton during fusion with hepatocytes |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5739296/ https://www.ncbi.nlm.nih.gov/pubmed/29074568 http://dx.doi.org/10.1091/mbc.E17-06-0400 |
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