The anti-DNA methylation mark histone H3 lysine 4 methylation recruits DNA demethylases in Arabidopsis [RNA-seq]
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PROVIDER: PRJNA1030747 | ENA |
REPOSITORIES: ENA
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Project description:The anti-DNA methylation mark histone H3 lysine 4 methylation recruits DNA demethylases in Arabidopsis [ChIP-seq]
| PRJNA1030746 | ENA
Project description:The anti-DNA methylation mark histone H3 lysine 4 methylation recruits DNA demethylases in Arabidopsis [WGBS, BS-PCR-seq]
| PRJNA1030748 | ENA
Project description:Patterning of DNA methylation in eukaryotic genomes is shaped by de novo methylation, maintenance mechanisms, and demethylation pathways, but how these processes interface with epigenetic modification of histones is poorly understood. We found that the targeting of histone H3 lysine four trimethylation (H3K4me3) with the catalytic domain of the SDG2 histone methyltransferase potently erased DNA methylation and gene silencing at FWA and other genes, and also erased CG DNA methylation in the transcribed region of genes. This methylation erasure was completely blocked in the ros1 dml2 dml3 triple mutant which eliminates DNA demethylation enzymes, showing that H3K4me3 promotes the active removal of DNA methylation rather than preventing CG methylation maintenance. We also found that targeting the removal of H3K4me3 with the novel protein TRBIP1, which acts in part by recruiting the H3K4me3 demethylase JMJ14, causes potent gene silencing. Furthermore, using a CRISPR-based system to simultaneously target both TRBIP1 and a CG specific DNA methyltransferase, we observed more potent establishment of DNA methylation and gene silencing than targeting the DNA methyltransferase by itself. These results highlight H3K4me3 as a potent anti-DNA methylation mark, and reveal potent and specific tools for epigenome engineering.
2025-01-13 | GSE245959 | GEO
Project description:Patterning of DNA methylation in eukaryotic genomes is shaped by de novo methylation, maintenance mechanisms, and demethylation pathways, but how these processes interface with epigenetic modification of histones is poorly understood. We found that the targeting of histone H3 lysine four trimethylation (H3K4me3) with the catalytic domain of the SDG2 histone methyltransferase potently erased DNA methylation and gene silencing at FWA and other genes, and also erased CG DNA methylation in the transcribed region of genes. This methylation erasure was completely blocked in the ros1 dml2 dml3 triple mutant which eliminates DNA demethylation enzymes, showing that H3K4me3 promotes the active removal of DNA methylation rather than preventing CG methylation maintenance. We also found that targeting the removal of H3K4me3 with the novel protein TRBIP1, which acts in part by recruiting the H3K4me3 demethylase JMJ14, causes potent gene silencing. Furthermore, using a CRISPR-based system to simultaneously target both TRBIP1 and a CG specific DNA methyltransferase, we observed more potent establishment of DNA methylation and gene silencing than targeting the DNA methyltransferase by itself. These results highlight H3K4me3 as a potent anti-DNA methylation mark, and reveal potent and specific tools for epigenome engineering.
2025-01-13 | GSE245958 | GEO
Project description:Patterning of DNA methylation in eukaryotic genomes is shaped by de novo methylation, maintenance mechanisms, and demethylation pathways, but how these processes interface with epigenetic modification of histones is poorly understood. We found that the targeting of histone H3 lysine four trimethylation (H3K4me3) with the catalytic domain of the SDG2 histone methyltransferase potently erased DNA methylation and gene silencing at FWA and other genes, and also erased CG DNA methylation in the transcribed region of genes. This methylation erasure was completely blocked in the ros1 dml2 dml3 triple mutant which eliminates DNA demethylation enzymes, showing that H3K4me3 promotes the active removal of DNA methylation rather than preventing CG methylation maintenance. We also found that targeting the removal of H3K4me3 with the novel protein TRBIP1, which acts in part by recruiting the H3K4me3 demethylase JMJ14, causes potent gene silencing. Furthermore, using a CRISPR-based system to simultaneously target both TRBIP1 and a CG specific DNA methyltransferase, we observed more potent establishment of DNA methylation and gene silencing than targeting the DNA methyltransferase by itself. These results highlight H3K4me3 as a potent anti-DNA methylation mark, and reveal potent and specific tools for epigenome engineering.
2025-01-13 | GSE245960 | GEO
Project description:Histone H3 lysine 4 methylation recruits DNA demethylases to enforce gene expression in Arabidopsis
| PRJNA1030744 | ENA
Project description:H3K36me2 recruits DNMT3A and shapes intergenic DNA methylation landscapes
| PRJNA486798 | ENA
Project description:DNA methylation is an epigenetic mark that is associated with transcriptional repression of transposable elements and protein coding genes. Conversely, transcriptionally active regulatory regions are strongly correlated with histone 3 lysine 4 di- and trimethylation (H3K4m2/3). We previously showed that Arabidopsis thaliana plants with mutations in the H3K4m2/m3 demethylase JUMONJI 14 (JMJ14) exhibit a mild reduction in RNA-directed DNA methylation (RdDM) that is associated with an increase in H3K4m2/m3 levels. To determine whether this incomplete RdDM reduction was the result of redundancy with other demethylases, we examined the genetic interaction of JMJ14 with another class of H3K4 demethylases: LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 1 and LYSINE-SPECIFIC DEMETHYLASE 1-LIKE 2 (LDL1 and LDL2). Genome-wide DNA methylation analyses reveal that both families impact RdDM, but not other DNA methylation pathways. ChIP-seq experiments show that regions that exhibit an observable DNA methylation decrease are co-incidental with increases in H3K4m2/m3. Interestingly, the impact on DNA methylation was stronger at DNA-methylated regions adjacent to H3K4m2/m3-marked protein coding genes, suggesting that the activity of H3K4 demethylases may be particularly crucial to prevent spreading of active epigenetic marks. Finally, RNA sequencing analyses indicate that at RdDM targets, the increase of H3K4m2/m3 is not generally associated with transcriptional de-repression. This suggests that the histone mark itself—not transcription—impacts the extent of RdDM.
2013-11-01 | GSE49090 | GEO
Project description:This is an observational, prospective study using fecal DNA methylation test to define the risk of suffering from advanced adenoma or colorectal cancer (CRC) compared to colonoscopy and fecal immunochemical test (FIT).
This study recruits at least 80 participants, including 40 people of healthy controls, 20 people with adenoma, and 20 people with CRC, which were confirmed by colonoscopy. All fecal specimens from participants will be examined by FIT and multi-methylated target gene detection through real-time quantitative methylation-specific PCR (qMSP).
The objective of this study is to evaluate the sensitivity and specificity of multi-methylated target PCR compared with the FIT and confirm the examination results through colonoscopy.
| 2372684 | ecrin-mdr-crc
Project description:We previously reported that gut microbiota induce de novo DNA methylation of the TLR4 gene in intestinal epithelial cells. Since DNA methyltransferase (DNMT) 3 mediates the transfer of methyl groups to any gene undergoing de novo methylation, the question of how gut microbiota induce the recruitment of DNMT3 to specific genes, including TLR4, remains to be addressed. In this study, we tried to identify an adaptor molecule that recruits DNMT3b to the TLR4 gene by comparing expression of DNMT3-interacting proteins between IEC lines with hypermethylated and hypomethylated TLR4 gene.
2023-03-11 | PXD035777 | Pride