Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA354264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5026641_1.fastq.gz | Fastqsanger.gz | |||
| SRR5026641_2.fastq.gz | Fastqsanger.gz | |||
| SRR5026642_1.fastq.gz | Fastqsanger.gz | |||
| SRR5026642_2.fastq.gz | Fastqsanger.gz |
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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
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.
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Project description:Bioinformatics powered correlative analysis of epigenomic patterns is an effective method to help derive biological hypotheses that can be tested genetically or biochemically. To accommodate the variety and complexity of epigenomic and transcriptomic patterns, ANchored COrrelative Patterns (ANCORP) was developed as a platform to integrate and intuitively visualize a large number of genome-wide profiles. With global profiles of 9 histone modifications mapped by ChIP-seq and a strand-specific RNA-seq dataset, we have applied the ANCORP-genetics pipeline for hypothesis building and testing in order to understand how global transcription may be regulated by epigenetic pathways such as histone modifications. It was found that intragenic antisense RNAs were depleted from genes with strong gene-body H3K36me2 mark and cytosine methylation enrichments but were significantly overrepresented in H3K4me3/H3K27me3 bivalent genes. Moreover, gene body H3K36me2 and DNA methylation anti-correlated with multiple active chromatin marks including H3K4me2/3, H3K9Ac and H3K18Ac. These observations lead us to hypothesize that H3K36me2 and DNA methylation may synergistically repress active chromatin marks in gene bodies and subsequently inhibit transcription of the antisense strand. Mutant analyses revealed that Polymerase Associated Factors (PAF) may be universally required for modulating NAT abundance whereas the role for the 5mC and H3K36me marks are more locus specific. H3K36me and PAF may either repress or permit the accumulation NATs depending on the chromatin state context in a particular transcription unit. Interestingly, the activation of antisense RNA in sdg8-2 or elf8-1 mutants does not associate with any increase of histone marks in gene bodies that are known to correlate with gene activation. Our results suggest that ANCORP-genetics is an effective approach to uncover epigenetic regulatory mechanisms by leveraging on the rapid advances in sequencing technologies and the resultant wealth of genome-wide information.
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Project description:Stress priming is a critical adaptive mechanism that enables plants to enhance responses to recurring environmental stresses. While transcriptomic changes associated with cold stress priming have been reported, the underlying epigenetic mechanisms remain largely unknown. In this study, we investigated transcriptomic and DNA methylation dynamics in cold-primed and non-primed Arabidopsis thaliana plants. Cold stress induces distinct gene expression patterns between primed and non-primed plants, accompanied by DNA methylation changes across all cytosine contexts in both protein-coding genes and transposable elements (TEs). Notably, CHH methylation within gene bodies and TEs is markedly reduced in cold-primed plants, suggesting a role for DNA hypomethylation in establishing cold stress memory. This hypomethylation correlates with decreased expression of the CMT2 DNA methyltransferase and components of the RNA-directed DNA methylation (RdDM) pathway, indicating a passive demethylation process during cold treatment. Furthermore, DNA methylation mutants exhibit enhanced cold stress memory, highlighting the role of methylation in preventing spurious gene activation and maintaining priming specificity. Particularly, met1, deficient in CG methylation, shows reduced methylation at the CBF gene cluster, correlating with their overexpression and enhanced activation of downstream cold-responsive genes. Our findings show that DNA methylation modulates cold stress memory by shaping chromatin and ensuring transcriptional precision.
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Project description:By relating the numbers of oxidized guanines in different sequence contexts to the abundance of these contexts in the human genome, we observed that the probability of guanine to be or remain oxidized is low if this guanine is preceded by cytosine (CpG sites) compared to other nucleotides. As CpG sites are substrates of epigenetic cytosine methylation, we investigated the influence of cytosine methylation status on guanine oxidation level in CpG sites. For this, we exposed HAP1 and U2OS cells for three days to GSK-3484862, a novel DNA methyltransferase 1 (DNMT1) inhibitor causing the degradation of this enzyme within 24 hours and having low cellular toxicity. Using Infinium MethylationEPIC v2.0 array, we observed a drastic hypomethylation after the exposure in both cell lines such that the peak of highly methylated CpG sites (beta values 0.8–1) found in vehicle (DMSO) exposed cells is absent in GSK-3484862-exposed cells. In contrast, the oxidation level of guanines in the CpG sites profiled by the array did not change in response to the inhibitor and was virtually constant across CpG sites with different methylation levels. In addition, on the level of all CpG sites in the genome, guanine-oxidation did not differ between DMSO and GSK-3484862 exposures. Thus, in CpG sites, guanine oxidation level likely does not depend on cytosine methylation status. As a control for the click-code-seq protocol, we successfully called 8-oxoG incorporated at specific sites in a plasmid (~25 fmol) that was mixed with ~28-times bigger amount of the unmodified vector. As a control for click-code-seq detection of abasic sites, we inserted uracils in a plasmid, converted them to abasic sites by uracil-DNA glycosylase (UDG) and successfully called them in the expected locations.
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Project description:Cytosine DNA methylation (mC) is a genome modification that can regulate the expression of coding and non-coding genetic elements. However, little is known about the involvement of mC in response to environmental cues. We performed whole genome bisulfite sequencing to assess the spatio-temporal dynamics of mC in Arabidopsis grown under phosphate starvation.
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Project description:DNA methylation plays a vital role in genome dynamics and, in the human genome, occurs predominantly at cytosine guanine dinucleotide (CpG) sites. The diploid haploid human genome analysed here contains around 2060 million CpG sites (methylome) where DNA methylation can vary, affecting many biological processes in health and disease. Using whole-genome bisulfite sequencing, we report the essentially complete (92.6282%) methylome of human peripheral blood mononuclear cells (PBMC) which constitute an important source for clinical blood tests world-wide. We find the majority of CpG sites (68.4% at false positive rate of 0.46%) and only <0.2% of non-CpG sites to be methylated, demonstrating that non-CpG cytosine methylation is negligible in human PBMC. Analysis of the PBMC methylome revealed a rich landscape of epigenomic data for 20 distinct features including regulatory, protein-coding, RNA gene coding, non-coding and repeat sequences. Alu element mobility, for instance, was found to negatively correlate with their methylation levels, emphasizing the critical role of DNA methylation in genome stability. Integration of our methylome data with the previously determined genome sequence of the same Asian individual analysed here, enabled a first assessment of allele-specific methylation (ASM) differences between the two haploid methylomes of any individual. Using a conservative cut-off (p <0.001), we identified 599 haploid differentially methylated regions (hDMRs) covering 287 genes. Of these, 76 genes had hDMRs within 2kb of their transcriptional start sites of which >80% displayed allele-specific expression (ASE) after random testing using TA clone sequencing of the same PBMC sample. These data show, that ASM is a recurrent phenomenon and highly correlated with ASE, suggesting that imprinting may be more common than previously thought. Our study not only provides a comprehensive resource for future epigenomic research but also demonstrates a paradigm of large-scale epigenomics studies through new sequencing technology. We report the essentially complete (92.6282%) methylome of human peripheral blood mononuclear cells (PBMC) which constitute an important source for clinical blood tests world-wide.
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Project description:Genome-wide, High Resolution DNA Methylation Profiling Using Bisulfite-Mediated Cytosine Conversion
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