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PLoS Genet. 2016 Sep 13;12(9):e1006298. doi: 10.1371/journal.pgen.1006298. eCollection 2016.

Nuclear Localised MORE SULPHUR ACCUMULATION1 Epigenetically Regulates Sulphur Homeostasis in Arabidopsis thaliana.

Author information

  • 1Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen, United Kingdom.
  • 2Botanical Institute, Cluster of Excellence on Plant Sciences (CEPLAS), University of Cologne, Cologne, Germany.
  • 3Centre for Organismal Studies Heidelberg, Heidelberg University, Heidelberg, Germany.
  • 4Department of Plant Physiology, University of Rostock, Rostock, Germany.
  • 5Institute of Biological Chemistry, Washington State University, Pullman, Washington, United States of America.
  • 6Department of Biochemistry, Purdue University, West Lafayette, Indiana, United States of America.

Abstract

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.

PMID:
27622452
PMCID:
PMC5021336
DOI:
10.1371/journal.pgen.1006298
[PubMed - in process]
Free PMC Article
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