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Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds

Sulphur deficiency in crops became an agricultural concern several decades ago, due to the decrease of S deposition and the atmospheric sulphur dioxide emissions released by industrial plants. Autophagy, which is a conserved mechanism for nutrient recycling in eukaryotes, is involved in nitrogen, ir...

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Autores principales: Lornac, Aurélia, Havé, Marien, Chardon, Fabien, Soulay, Fabienne, Clément, Gilles, Avice, Jean-Christophe, Masclaux-Daubresse, Céline
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073174/
https://www.ncbi.nlm.nih.gov/pubmed/32023971
http://dx.doi.org/10.3390/cells9020332
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author Lornac, Aurélia
Havé, Marien
Chardon, Fabien
Soulay, Fabienne
Clément, Gilles
Avice, Jean-Christophe
Masclaux-Daubresse, Céline
author_facet Lornac, Aurélia
Havé, Marien
Chardon, Fabien
Soulay, Fabienne
Clément, Gilles
Avice, Jean-Christophe
Masclaux-Daubresse, Céline
author_sort Lornac, Aurélia
collection PubMed
description Sulphur deficiency in crops became an agricultural concern several decades ago, due to the decrease of S deposition and the atmospheric sulphur dioxide emissions released by industrial plants. Autophagy, which is a conserved mechanism for nutrient recycling in eukaryotes, is involved in nitrogen, iron, zinc and manganese remobilizations from the rosette to the seeds in Arabidopsis thaliana. Here, we have compared the role of autophagy in sulphur and nitrogen management at the whole plant level, performing concurrent labelling with (34)S and (15)N isotopes on atg5 mutants and control lines. We show that both (34)S and (15)N remobilizations from the rosette to the seeds are impaired in the atg5 mutants irrespective of salicylic acid accumulation and of sulphur nutrition. The comparison in each genotype of the partitions of (15)N and (34)S in the seeds (as % of the whole plant) indicates that the remobilization of (34)S to the seeds was twice more efficient than that of (15)N in both autophagy mutants and control lines under high S conditions, and also in control lines under low S conditions. This was different in the autophagy mutants grown under low S conditions. Under low S, the partition of (34)S to their seeds was indeed not twice as high but similar to that of (15)N. Such discrepancy shows that when sulphate availability is scarce, autophagy mutants display stronger defects for (34)S remobilization relative to (15)N remobilization than under high S conditions. It suggests, moreover, that autophagy mainly affects the transport of N-poor S-containing molecules and possibly sulphate.
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spelling pubmed-70731742020-03-19 Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds Lornac, Aurélia Havé, Marien Chardon, Fabien Soulay, Fabienne Clément, Gilles Avice, Jean-Christophe Masclaux-Daubresse, Céline Cells Article Sulphur deficiency in crops became an agricultural concern several decades ago, due to the decrease of S deposition and the atmospheric sulphur dioxide emissions released by industrial plants. Autophagy, which is a conserved mechanism for nutrient recycling in eukaryotes, is involved in nitrogen, iron, zinc and manganese remobilizations from the rosette to the seeds in Arabidopsis thaliana. Here, we have compared the role of autophagy in sulphur and nitrogen management at the whole plant level, performing concurrent labelling with (34)S and (15)N isotopes on atg5 mutants and control lines. We show that both (34)S and (15)N remobilizations from the rosette to the seeds are impaired in the atg5 mutants irrespective of salicylic acid accumulation and of sulphur nutrition. The comparison in each genotype of the partitions of (15)N and (34)S in the seeds (as % of the whole plant) indicates that the remobilization of (34)S to the seeds was twice more efficient than that of (15)N in both autophagy mutants and control lines under high S conditions, and also in control lines under low S conditions. This was different in the autophagy mutants grown under low S conditions. Under low S, the partition of (34)S to their seeds was indeed not twice as high but similar to that of (15)N. Such discrepancy shows that when sulphate availability is scarce, autophagy mutants display stronger defects for (34)S remobilization relative to (15)N remobilization than under high S conditions. It suggests, moreover, that autophagy mainly affects the transport of N-poor S-containing molecules and possibly sulphate. MDPI 2020-01-31 /pmc/articles/PMC7073174/ /pubmed/32023971 http://dx.doi.org/10.3390/cells9020332 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Lornac, Aurélia
Havé, Marien
Chardon, Fabien
Soulay, Fabienne
Clément, Gilles
Avice, Jean-Christophe
Masclaux-Daubresse, Céline
Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title_full Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title_fullStr Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title_full_unstemmed Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title_short Autophagy Controls Sulphur Metabolism in the Rosette Leaves of Arabidopsis and Facilitates S Remobilization to the Seeds
title_sort autophagy controls sulphur metabolism in the rosette leaves of arabidopsis and facilitates s remobilization to the seeds
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7073174/
https://www.ncbi.nlm.nih.gov/pubmed/32023971
http://dx.doi.org/10.3390/cells9020332
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