Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana
Sulphur (S) is an essential element for all living organisms. The uptake, assimilation and metabolism of S in plants are well studied. However, the regulation of S homeostasis remains largely unknown. Here, we report on the identification and characterisation of the more sulphur accumulation1 (msa1-...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
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Public Library of Science
2016
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| Online Access: | https://eprints.nottingham.ac.uk/37474/ |
| _version_ | 1848795466885496832 |
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| author | Huang, Xin-Yuan Chao, Dai-Yin Koprivova, Anna Danku, John Wirtz, Markus Müller, Steffen Sandoval, Francisco J. Bauwe, Hermann Roje, Sanja Dilkes, Brian Hell, Rüdiger Kopriva, Stanislav Salt, David E. |
| author_facet | Huang, Xin-Yuan Chao, Dai-Yin Koprivova, Anna Danku, John Wirtz, Markus Müller, Steffen Sandoval, Francisco J. Bauwe, Hermann Roje, Sanja Dilkes, Brian Hell, Rüdiger Kopriva, Stanislav Salt, David E. |
| author_sort | Huang, Xin-Yuan |
| building | Nottingham Research Data Repository |
| collection | Online Access |
| description | Sulphur (S) is an essential element for all living organisms. The uptake, assimilation and metabolism of S in plants are well studied. However, the regulation of S homeostasis remains largely unknown. Here, we report on the identification and characterisation of the more sulphur accumulation1 (msa1-1) mutant. The MSA1 protein is localized to the nucleus and is required for both S adenosylmethionine (SAM) production and DNA methylation. Loss of function of the nuclear localised MSA1 leads to a reduction in SAM in roots and a strong S-deficiency response even at ample S supply, causing an over- accumulation of sulphate, sulphite, cysteine and glutathione. Supplementation with SAM suppresses this high S phenotype. Furthermore, mutation of MSA1 affects genome-wide DNA methylation, including the methylation of S-deficiency responsive genes. Elevated S accumulation in msa1-1 requires the increased expression of the sulphate transporter genes SULTR1;1 and SULTR1;2 which are also differentially methylated in msa1-1. Our results suggest a novel function for MSA1 in the nucleus in regulating SAM biosynthesis and maintaining S homeostasis epigenetically via DNA methylation. |
| first_indexed | 2025-11-14T19:32:32Z |
| format | Article |
| id | nottingham-37474 |
| institution | University of Nottingham Malaysia Campus |
| institution_category | Local University |
| last_indexed | 2025-11-14T19:32:32Z |
| publishDate | 2016 |
| publisher | Public Library of Science |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | nottingham-374742020-05-04T18:12:36Z https://eprints.nottingham.ac.uk/37474/ Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana Huang, Xin-Yuan Chao, Dai-Yin Koprivova, Anna Danku, John Wirtz, Markus Müller, Steffen Sandoval, Francisco J. Bauwe, Hermann Roje, Sanja Dilkes, Brian Hell, Rüdiger Kopriva, Stanislav Salt, David E. Sulphur (S) is an essential element for all living organisms. The uptake, assimilation and metabolism of S in plants are well studied. However, the regulation of S homeostasis remains largely unknown. Here, we report on the identification and characterisation of the more sulphur accumulation1 (msa1-1) mutant. The MSA1 protein is localized to the nucleus and is required for both S adenosylmethionine (SAM) production and DNA methylation. Loss of function of the nuclear localised MSA1 leads to a reduction in SAM in roots and a strong S-deficiency response even at ample S supply, causing an over- accumulation of sulphate, sulphite, cysteine and glutathione. Supplementation with SAM suppresses this high S phenotype. Furthermore, mutation of MSA1 affects genome-wide DNA methylation, including the methylation of S-deficiency responsive genes. Elevated S accumulation in msa1-1 requires the increased expression of the sulphate transporter genes SULTR1;1 and SULTR1;2 which are also differentially methylated in msa1-1. Our results suggest a novel function for MSA1 in the nucleus in regulating SAM biosynthesis and maintaining S homeostasis epigenetically via DNA methylation. Public Library of Science 2016-09-13 Article PeerReviewed Huang, Xin-Yuan, Chao, Dai-Yin, Koprivova, Anna, Danku, John, Wirtz, Markus, Müller, Steffen, Sandoval, Francisco J., Bauwe, Hermann, Roje, Sanja, Dilkes, Brian, Hell, Rüdiger, Kopriva, Stanislav and Salt, David E. (2016) Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana. PLoS Genetics, 12 (9). e1006298/1-e1006298/29. ISSN 1553-7404 http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1006298 doi:10.1371/journal.pgen.1006298 doi:10.1371/journal.pgen.1006298 |
| spellingShingle | Huang, Xin-Yuan Chao, Dai-Yin Koprivova, Anna Danku, John Wirtz, Markus Müller, Steffen Sandoval, Francisco J. Bauwe, Hermann Roje, Sanja Dilkes, Brian Hell, Rüdiger Kopriva, Stanislav Salt, David E. Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title | Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title_full | Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title_fullStr | Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title_full_unstemmed | Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title_short | Nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in Arabidopsis thaliana |
| title_sort | nuclear localised more sulphur accumulation1 epigenetically regulates sulphur homeostasis in arabidopsis thaliana |
| url | https://eprints.nottingham.ac.uk/37474/ https://eprints.nottingham.ac.uk/37474/ https://eprints.nottingham.ac.uk/37474/ |