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RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling
Growth of eukaryotic cells is regulated by the target of rapamycin (TOR). The strongest activator of TOR in metazoa is amino acid availability. The established transducers of amino acid sensing to TOR in metazoa are absent in plants. Hence, a fundamental question is how amino acid sensing is achieve...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5660089/ https://www.ncbi.nlm.nih.gov/pubmed/29079776 http://dx.doi.org/10.1038/s41467-017-01224-w |
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author | Dong, Yihan Silbermann, Marleen Speiser, Anna Forieri, Ilaria Linster, Eric Poschet, Gernot Allboje Samami, Arman Wanatabe, Mutsumi Sticht, Carsten Teleman, Aurelio A. Deragon, Jean-Marc Saito, Kazuki Hell, Rüdiger Wirtz, Markus |
author_facet | Dong, Yihan Silbermann, Marleen Speiser, Anna Forieri, Ilaria Linster, Eric Poschet, Gernot Allboje Samami, Arman Wanatabe, Mutsumi Sticht, Carsten Teleman, Aurelio A. Deragon, Jean-Marc Saito, Kazuki Hell, Rüdiger Wirtz, Markus |
author_sort | Dong, Yihan |
collection | PubMed |
description | Growth of eukaryotic cells is regulated by the target of rapamycin (TOR). The strongest activator of TOR in metazoa is amino acid availability. The established transducers of amino acid sensing to TOR in metazoa are absent in plants. Hence, a fundamental question is how amino acid sensing is achieved in photo-autotrophic organisms. Here we demonstrate that the plant Arabidopsis does not sense the sulfur-containing amino acid cysteine itself, but its biosynthetic precursors. We identify the kinase GCN2 as a sensor of the carbon/nitrogen precursor availability, whereas limitation of the sulfur precursor is transduced to TOR by downregulation of glucose metabolism. The downregulated TOR activity caused decreased translation, lowered meristematic activity, and elevated autophagy. Our results uncover a plant-specific adaptation of TOR function. In concert with GCN2, TOR allows photo-autotrophic eukaryotes to coordinate the fluxes of carbon, nitrogen, and sulfur for efficient cysteine biosynthesis under varying external nutrient supply. |
format | Online Article Text |
id | pubmed-5660089 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-56600892017-10-31 RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling Dong, Yihan Silbermann, Marleen Speiser, Anna Forieri, Ilaria Linster, Eric Poschet, Gernot Allboje Samami, Arman Wanatabe, Mutsumi Sticht, Carsten Teleman, Aurelio A. Deragon, Jean-Marc Saito, Kazuki Hell, Rüdiger Wirtz, Markus Nat Commun Article Growth of eukaryotic cells is regulated by the target of rapamycin (TOR). The strongest activator of TOR in metazoa is amino acid availability. The established transducers of amino acid sensing to TOR in metazoa are absent in plants. Hence, a fundamental question is how amino acid sensing is achieved in photo-autotrophic organisms. Here we demonstrate that the plant Arabidopsis does not sense the sulfur-containing amino acid cysteine itself, but its biosynthetic precursors. We identify the kinase GCN2 as a sensor of the carbon/nitrogen precursor availability, whereas limitation of the sulfur precursor is transduced to TOR by downregulation of glucose metabolism. The downregulated TOR activity caused decreased translation, lowered meristematic activity, and elevated autophagy. Our results uncover a plant-specific adaptation of TOR function. In concert with GCN2, TOR allows photo-autotrophic eukaryotes to coordinate the fluxes of carbon, nitrogen, and sulfur for efficient cysteine biosynthesis under varying external nutrient supply. Nature Publishing Group UK 2017-10-27 /pmc/articles/PMC5660089/ /pubmed/29079776 http://dx.doi.org/10.1038/s41467-017-01224-w Text en © The Author(s) 2017 https://creativecommons.org/licenses/by/4.0/ Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Dong, Yihan Silbermann, Marleen Speiser, Anna Forieri, Ilaria Linster, Eric Poschet, Gernot Allboje Samami, Arman Wanatabe, Mutsumi Sticht, Carsten Teleman, Aurelio A. Deragon, Jean-Marc Saito, Kazuki Hell, Rüdiger Wirtz, Markus RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title | RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title_full | RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title_fullStr | RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title_full_unstemmed | RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title_short | RETRACTED ARTICLE: Sulfur availability regulates plant growth via glucose-TOR signaling |
title_sort | retracted article: sulfur availability regulates plant growth via glucose-tor signaling |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5660089/ https://www.ncbi.nlm.nih.gov/pubmed/29079776 http://dx.doi.org/10.1038/s41467-017-01224-w |
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