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Methyl DIP-chip from self-pollinated ddm1 mutant and ddm1 kyp double mutant

ABSTRACT: Methylation of histone H3 lysine 9 (H3K9me) and small RNA are associated with constitutively silent chromatin in diverse eukaryotes including plants. In plants, silent transposons are also marked by cytosine methylation, especially at non-CpG sites. The transposon-specific non-CpG methylation in plants is controlled by small RNA and H3K9me. Although it is often assumed that small RNA directs H3K9me,　interaction between small RNA and H3K9me has not been directly shown in plants. We have previously shown that a mutation in a chromatin remodeling gene DDM1 (decrease in DNA methylation) induces a global decrease as well as local increase of cytosine methylation and accumulation of small RNA in a locus called BONSAI. Here we show that the de novo BONSAI methylation does not depend on RNAi but depends on H3K9me. Notably, in mutant of H3K9 methylase gene KRYPTONITE or H3K9me-dependent DNA methylase gene CHROMOMETHYALSE3, the ddm1-induced de novo cytosine methylation was abolished for all three contexts, CpG, CpHpG, and CpHpH. Furthermore, RNAi mutants showed strong developmental defects when combined with ddm1 mutation. Our results revealed unexpected interactions of epigenetic modifications, which could be conserved among diverse eukaryotes.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE34222 | GEO | 2011/12/25

SECONDARY ACCESSION(S): PRJNA149817

REPOSITORIES: GEO

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Methyl DIP-chip from self-pollinated ddm1 mutant and ddm1 kyp double mutant

Project description:Methylation of histone H3 lysine 9 (H3K9me) and small RNA are associated with constitutively silent chromatin in diverse eukaryotes including plants. In plants, silent transposons are also marked by cytosine methylation, especially at non-CpG sites. The transposon-specific non-CpG methylation in plants is controlled by small RNA and H3K9me. Although it is often assumed that small RNA directs H3K9me,　interaction between small RNA and H3K9me has not been directly shown in plants. We have previously shown that a mutation in a chromatin remodeling gene DDM1 (decrease in DNA methylation) induces a global decrease as well as local increase of cytosine methylation and accumulation of small RNA in a locus called BONSAI. Here we show that the de novo BONSAI methylation does not depend on RNAi but depends on H3K9me. Notably, in mutant of H3K9 methylase gene KRYPTONITE or H3K9me-dependent DNA methylase gene CHROMOMETHYALSE3, the ddm1-induced de novo cytosine methylation was abolished for all three contexts, CpG, CpHpG, and CpHpH. Furthermore, RNAi mutants showed strong developmental defects when combined with ddm1 mutation. Our results revealed unexpected interactions of epigenetic modifications, which could be conserved among diverse eukaryotes. comparison of DNA methylation between WT, 2G ddm1 (2 replications), 8G ddm1 (2 replications), and 8G ddm1 kyp

2011-12-25 | E-GEOD-34222 | biostudies-arrayexpress

Genome-wide analysis of H3K9me2 in ibm1, kyp, and cmt3 mutants of Arabidopsis thaliana

Project description:In diverse eukaryotes, constitutively silent sequences, such as transposons and repeats, are marked by methylation at histone H3 lysine 9 (H3K9me). Despites the conservation and importance in the genome integrity, mechanisms to exclude H3K9m from active genes remained largely unexplored. Here we show in Arabidopsis that the exclusion depends on a histone demethylase gene, IBM1 (increase in BONSAI methylation); loss-of-function ibm1 mutation caused ectopic H3K9me in thousands of genes, which accompanies genic DNA methylation at non-CG sites. The ibm1-induced genic H3K9me depended on both histone methylase KYP/SUVH4 and DNA methylase CMT3, suggesting interdependence of two epigenetic marks – H3K9me and non-CG methylation. Notably, IBM1 enhanced loss of H3K9m in transcriptionally de-repressed sequences. Furthermore, disruption of transcription in genes induced ectopic non-CG methylation, mimicking the loss of IBM1 function. We propose that active chromatin is stabilized by the autocatalytic loop of transcription and H3K9 demethylation. This process counteracts accumulation of silent epigenetic marks, H3K9me and non-CG methylation, which is also autocatalytic. Leaves of 4-week-old plants were fixed as described previously (Saze et al, 2008). Chromatin immunoprecipitation (ChIP) was performed as described previously (Kimura et al, 2008), using antibody against H3K9me2 (CMA307, Kimura et al, 2008, PMID: 18227620). Non-immunoprecipitated DNA (input DNA) and ChIP samples were amplified, labeled, and hybridized to microarray according to the manufacturer’s instruction (Protocols for Chromatin Immunoprecipitation and Amplification, NimbleGen). Input DNA and ChIP DNA were differentially labeled with Cy3 and Cy5, respectively, and competitively hybridized to a microarray chip. We used NimbleGen 2.1M HD2 array covering entire genome of A. thaliana.

2010-09-21 | E-GEOD-22953 | biostudies-arrayexpress

DDM1 and RdDM are the major regulators of transposon DNA methylation in Arabidopsis

Project description:Eukaryotic DNA methylation is found in silent transposable elements and active genes. Nucleosome remodelers of the DDM1/Lsh family are thought to be specifically required to maintain transposon methylation, but the reason for this is unknown. Here, we find that a chromatin gradient that extends from the most heterochromatic transposons to euchromatic genes determines the requirement of DDM1 for methylation maintenance in all sequence contexts. We also show that small RNA-directed DNA methylation (RdDM) is inhibited by heterochromatin and absolutely requires the nucleosome remodeler DRD1. DDM1 and RdDM independently mediate nearly all transposon methylation, which is catalyzed by the methyltransferases MET1 (CG), CMT3 (CHG), DRM2 (CHH) and CMT2 (CHH), and collaborate to repress transposition and regulate the methylation and expression of genes. Our results indicate that the Arabidopsis genome is defined by a heterochromatic continuum that governs the access of DNA methyltransferases and potentially all DNA binding proteins. Examination of DNA methylation, transcription and nucleosomes in Arabidopsis wild-type and/or ddm1, RdDM and DNA methylase mutants.

2013-04-17 | E-GEOD-41302 | biostudies-arrayexpress

Genome-wide analysis of H3K9me2 in ibm1, kyp, and cmt3 mutants of Arabidopsis thaliana

2010-09-21 | GSE22953 | GEO

mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana

Project description:mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana seedlings and bolting plants. Features found to be significantly enriched for DNA methylation were determined. This SuperSeries is composed of the following subset Series: GSE1324: EV23+24 mRNA levels in Wild-type versus ddm1/+ backcross bolting Arabidopsis thaliana plants GSE1325: EV33+34 mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana seedlings GSE1326: VC109+111 mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana seedlings GSE1327: EV39+40 mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana seedlings GSE1328: VC110+112 mRNA levels in Wild-type versus ddm1 bolting Arabidopsis thaliana plants Refer to individual Series

2010-06-09 | E-GEOD-1354 | biostudies-arrayexpress

mRNA levels in Wild-type versus ddm1 Arabidopsis thaliana

2004-06-12 | GSE1354 | GEO

DDM1-mediated gene body DNA methylation is associated with inducible activation of defense-related genes in Arabidopsis [expression]

Project description:Background: Plants memorize previous pathogen attacks and are ‘primed’ to produce a faster and stronger defense response, which is critical for defense against pathogens. In plants, cytosines in transposons and gene bodies are reported to be frequently methylated. Demethylation of transposons can affect disease resistance by regulating the transcription of nearby genes during defense response, but the role of gene body methylation (GBM) in defense responses remains unclear. Results: Here, we find that loss of the chromatin remodeler decrease in DNA methylation 1 (ddm1) synergistically enhances resistance to a biotrophic pathogen under mild chemical priming. DDM1 mediates gene body methylation at a subset of stress-responsive genes with distinct chromatin properties from conventional gene body methylated genes. Decreased gene body methylation in loss of ddm1 mutant is associated with hyperactivation of these gene body methylated genes. Knockout of glyoxysomal protein kinase 1 (gpk1), a hypomethylated gene in ddm1 loss of function mutant, impairs priming of defense response to pathogen infection in Arabidopsis. We also find that DDM1-mediated gene body methylation is prone to epigenetic variation among natural Arabidopsis populations, and GPK1 expression is hyperactivated in natural variants with demethylated GPK1. Conclusions: Based on our collective results, we propose that DDM1-mediated GBM provides a possible regulatory axis for plants to modulate the inducibility of the immune response.

2023-04-14 | GSE59914 | GEO

DDM1-mediated gene body DNA methylation is associated with inducible activation of defense-related genes in Arabidopsis [DNA methylation]

2023-04-14 | GSE98162 | GEO

WGBS of 169 ddm1-derived epiRILs

Project description:169 ddm1-derived epigenetic recombinant inbred lines (epiRILs) were obtained from the Versailles Arabidopsis Stock center of INRA (http://publiclines.versailles.inra.fr/) and they were propagated in a fully automatic phenotyping facility for small plants at the Leibniz Institute of Plant Genetics and Crop Plant Research (IPK). Whole Genome Bisulphite Sequencing was performed at the Beijing Genome Institute.

2021-10-07 | GSE171414 | GEO

The chromatin remodeler protein DDM1 regulates early seedling growth hybrid vigor by modulating gene expression in Arabidopsis

Project description:Despite of the paramount importance of heterosis in agriculture, the molecular mechanisms underlying heterosis remain elusive. Recent studies in Arabidopsis suggested possible involvement of DNA methylation in heterosis. We tested this hypothesis genetically by crossing homozygous mutants in DNA methylation-related genes in the Columbia (Col) ecotype with homozygous mutants in the same DNA methylation-related genes in the C24 ecotype. When genes in the RNA-directed DNA methylation (RdDM) pathway were mutated, the resultant F1 hybrids did not show appreciable loss of best parent heterosis (BPH) performances in early seedling growth. In contrast, mutations in the putative chromatin remodeling protein DECREASE OF DNA METHYLATION 1 (DDM1) caused ddm1-Col like growth pattern of ddm1-F1 hybrids, a mid-parent heterosis (MPH) performance. To understand the underlying molecular mechanisms, we compared the transcriptomes of the parental plants and reciprocal F1 hybrids in the wild type and ddm1 mutant backgrounds, and identified 183 non-additively expressed (NAE) genes, which were functionally enriched in defense response, a group of genes negatively associated with plant size. Interestingly, for the expression levels of the NAE genes, WT-F1 hybrids were enriched in the Golden Ration between mid-parent values (MPVs) and Col parents in WT, but ddm1-F1 hybrids were comparable to ddm1-Col parent in ddm1 mutant, which explained the MPH performance of ddm1-F1 hybrids. DNA methylation analyses revealed only one third of the NAE genes with highly methylated promoters whose expression is negatively associated with DNA methylation of promoters, strongly suggesting that DDM1 regulates heterosis by multiple epigenetic modifications.

2016-11-07 | GSE74551 | GEO

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