Welcome to the UPF Digital Repository

Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1

Show simple item record

dc.contributor.author Cruz Garcia, David
dc.contributor.author Brouwers, Nathalie
dc.contributor.author Malhotra, Vivek
dc.contributor.author Curwin, Amy
dc.date.accessioned 2020-05-14T06:49:02Z
dc.date.issued 2020
dc.identifier.citation Cruz-Garcia D, Brouwers N, Malhotra V, Curwin AJ. Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1. J Cell Biol. 2020; 219(4). pii: e201905028. DOI: 10.1083/jcb.201905028
dc.identifier.issn 0021-9525
dc.identifier.uri http://hdl.handle.net/10230/44538
dc.description.abstract 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.
dc.description.sponsorship This work was funded by grants from the Spanish Ministry of Economy and Competitiveness (BFU2013-44188-P and BFU2016_75372-P to V. Malhotra). We acknowledge support of the Spanish Ministry of Economy, Industry and Competitiveness to the European Molecular Biology Laboratories (EMBL) partnership, the Programmes “Centro de Excelencia Severo Ochoa 2013–2017” (SEV-2012-0208 and SEV-2013-0347), and the Centres de Recerca de Catalunya (CERCA) Program/Generalitat de Catalunya. The mass spectrometry data were acquired at the Centre for Genomic Regulation/UPF Proteomics Unit, which is part of Proteored, PRB3, and is funded by El Instituto de Salud Carlos III (ISCIII) and European Regional Development Fund (ERDF; grant PT17/0019 of the PE I+D+i 2013–2016).
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Rockefeller University Press
dc.relation.ispartof J Cell Biol. 2020; 219(4). pii: e201905028
dc.rights © 2020 Cruz-Garcia et al. 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/).
dc.rights.uri https://creativecommons.org/licenses/by-nc-sa/4.0/
dc.title Reactive oxygen species triggers unconventional secretion of antioxidants and Acb1
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1083/jcb.201905028
dc.subject.keyword Cell metabolism
dc.subject.keyword Metabolism
dc.subject.keyword Physiology
dc.subject.keyword Trafficking
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PE/BFU2013-44188-P
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PE/BFU2016-75372-P
dc.rights.accessRights info:eu-repo/semantics/embargoedAccess
dc.type.version info:eu-repo/semantics/publishedVersion
dc.embargo.liftdate 2020-10-06
dc.date.embargoEnd info:eu-repo/date/embargoEnd/2020-10-06

Blocked

This item appears in the following Collection(s)

Show simple item record

Search DSpace


Advanced Search

Browse

My Account

Statistics

Compliant to Partaking