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Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Nutrient deprivation triggers the release of signal-sequence–lacking Acb1 and the antioxidant superoxide dismutase 1 (SOD1). We now report that secreted SOD1 is functionally active and accompanied by export of other antioxidant enzymes such as thioredoxins (Trx1 and Trx2) and peroxiredoxin Ahp1 in a...

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Autores principales: Cruz-Garcia, David, Brouwers, Nathalie, Malhotra, Vivek, Curwin, Amy J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Rockefeller University Press 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147093/
https://www.ncbi.nlm.nih.gov/pubmed/32328640
http://dx.doi.org/10.1083/jcb.201905028
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author Cruz-Garcia, David
Brouwers, Nathalie
Malhotra, Vivek
Curwin, Amy J.
author_facet Cruz-Garcia, David
Brouwers, Nathalie
Malhotra, Vivek
Curwin, Amy J.
author_sort Cruz-Garcia, David
collection PubMed
description Nutrient deprivation triggers the release of signal-sequence–lacking Acb1 and the antioxidant superoxide dismutase 1 (SOD1). We now report that secreted SOD1 is functionally active and accompanied by export of other antioxidant enzymes such as thioredoxins (Trx1 and Trx2) and peroxiredoxin Ahp1 in a Grh1-dependent manner. Our data reveal that starvation leads to production of nontoxic levels of reactive oxygen species (ROS). Treatment of cells with N-acetylcysteine (NAC), which sequesters ROS, prevents antioxidants and Acb1 secretion. Starved cells lacking Grh1 are metabolically active, but defective in their ability to regrow upon return to growth conditions. Treatment with NAC restored the Grh1-dependent effect of starvation on cell growth. In sum, starvation triggers ROS production and cells respond by secreting antioxidants and the lipogenic signaling protein Acb1. We suggest that starvation-specific unconventional secretion of antioxidants and Acb1-like activities maintain cells in a form necessary for growth upon their eventual return to normal conditions.
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spelling pubmed-71470932020-10-06 Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1 Cruz-Garcia, David Brouwers, Nathalie Malhotra, Vivek Curwin, Amy J. J Cell Biol Report Nutrient deprivation triggers the release of signal-sequence–lacking Acb1 and the antioxidant superoxide dismutase 1 (SOD1). We now report that secreted SOD1 is functionally active and accompanied by export of other antioxidant enzymes such as thioredoxins (Trx1 and Trx2) and peroxiredoxin Ahp1 in a Grh1-dependent manner. Our data reveal that starvation leads to production of nontoxic levels of reactive oxygen species (ROS). Treatment of cells with N-acetylcysteine (NAC), which sequesters ROS, prevents antioxidants and Acb1 secretion. Starved cells lacking Grh1 are metabolically active, but defective in their ability to regrow upon return to growth conditions. Treatment with NAC restored the Grh1-dependent effect of starvation on cell growth. In sum, starvation triggers ROS production and cells respond by secreting antioxidants and the lipogenic signaling protein Acb1. We suggest that starvation-specific unconventional secretion of antioxidants and Acb1-like activities maintain cells in a form necessary for growth upon their eventual return to normal conditions. Rockefeller University Press 2020-03-19 /pmc/articles/PMC7147093/ /pubmed/32328640 http://dx.doi.org/10.1083/jcb.201905028 Text en © 2020 Cruz-Garcia et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Report
Cruz-Garcia, David
Brouwers, Nathalie
Malhotra, Vivek
Curwin, Amy J.
Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title_full Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title_fullStr Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title_full_unstemmed Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title_short Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
title_sort reactive oxygen species triggers unconventional secretion of antioxidants and acb1
topic Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7147093/
https://www.ncbi.nlm.nih.gov/pubmed/32328640
http://dx.doi.org/10.1083/jcb.201905028
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