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GSNOR Contributes to Demethylation and Expression of Transposable Elements and Stress-Responsive Genes
- Source :
- Antioxidants, Volume 10, Issue 7, Antioxidants, Vol 10, Iss 1128, p 1128 (2021), Antioxidants 10:1128 (2021)
- Publication Year :
- 2021
- Publisher :
- Multidisciplinary Digital Publishing Institute, 2021.
-
Abstract
- In the past, reactive nitrogen species (RNS) were supposed to be stress-induced by-products of disturbed metabolism that cause oxidative damage to biomolecules. However, emerging evidence demonstrates a substantial role of RNS as endogenous signals in eukaryotes. In plants, S-nitrosoglutathione (GSNO) is the dominant RNS and serves as the •NO donor for S-nitrosation of diverse effector proteins. Remarkably, the endogenous GSNO level is tightly controlled by S-nitrosoglutathione reductase (GSNOR) that irreversibly inactivates the glutathione-bound NO to ammonium. Exogenous feeding of diverse RNS, including GSNO, affected chromatin accessibility and transcription of stress-related genes, but the triggering function of RNS on these regulatory processes remained elusive. Here, we show that GSNO reductase-deficient plants (gsnor1-3) accumulate S-adenosylmethionine (SAM), the principal methyl donor for methylation of DNA and histones. This SAM accumulation triggered a substantial increase in the methylation index (MI = [SAM]/[S-adenosylhomocysteine]), indicating the transmethylation activity and histone methylation status in higher eukaryotes. Indeed, a mass spectrometry-based global histone profiling approach demonstrated a significant global increase in H3K9me2, which was independently verified by immunological detection using a selective antibody. Since H3K9me2-modified regions tightly correlate with methylated DNA regions, we also determined the DNA methylation status of gsnor1-3 plants by whole-genome bisulfite sequencing. DNA methylation in the CG, CHG, and CHH contexts in gsnor1-3 was significantly enhanced compared to the wild type. We propose that GSNOR1 activity affects chromatin accessibility by controlling the transmethylation activity (MI) required for maintaining DNA methylation and the level of the repressive chromatin mark H3K9me2.
- Subjects :
- 0106 biological sciences
0301 basic medicine
Physiology
Clinical Biochemistry
Bisulfite sequencing
S-adenosylhomocysteine
Dna Methylation
Histone Methylation
Metaboloepigenetic
Nitric Oxide
S-nitrosoglutathione
S-nitrosoglutathione Reductase
RM1-950
01 natural sciences
Biochemistry
Article
03 medical and health sciences
chemistry.chemical_compound
nitric oxide
Histone methylation
histone methylation
Molecular Biology
S-nitrosoglutathione reductase
DNA methylation
biology
Chemistry
Cell Biology
Methylation
Chromatin
Cell biology
metaboloepigenetic
030104 developmental biology
Histone
biology.protein
Therapeutics. Pharmacology
Transmethylation
DNA
010606 plant biology & botany
Subjects
Details
- Language :
- English
- ISSN :
- 20763921
- Database :
- OpenAIRE
- Journal :
- Antioxidants
- Accession number :
- edsair.doi.dedup.....8ef769d19bc1aaaa3cf4f249d97e60b7
- Full Text :
- https://doi.org/10.3390/antiox10071128