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The site-mutated Ehd3 failed to rescue the aberrant H3K36me2/me3 distribution patterns in the ehd3-1 mutant background.

ABSTRACT: We examined the genome-wide occupancy of H3K36me2/H3K36me3 in the transgenic plants HA-Ehd3/ehd3-1-1 and HA-Ehd3mu/ehd3-1-1.

ORGANISM(S): Oryza sativa

PROVIDER: GSE311864 | GEO | 2026/01/26

REPOSITORIES: GEO

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Similar Datasets

The site-mutated Ehd3 failed to rescue the aberrant H3K36me2/me3 distribution patterns in the ehd3-1 mutant background.

Project description:The site-mutated Ehd3 failed to rescue the aberrant H3K36me2/me3 distribution patterns in the ehd3-1 mutant background.

| PRJNA1371868 | ENA

Transcriptome data (mRNA-seq) for NiP, ehd3-1, sdg724-1, and ehd3 sdg724.

Project description:To explore how Ehd3 and SDG724 regulate gene transcription at the genome-wide level, we conducted RNA-seq analyses of NiP, ehd3-1, sdg724-1, and ehd3 sdg724.

2026-01-26 | GSE266906 | GEO

H3K4me1 directs H3K36me2 and H3K36me3 deposition in land plants

Project description:Monomethylation of histone H3 lysine 4 (H3K4me1) marks enhancers in mammals. However, the function of H3K4me1 in plants remains largely unclear. Here, we analyzed the genome-wide distribution of H3K4me1 in diverse species across evolution, revealing a distinctive H3K4me1 distribution pattern in land plants. To explore the function of H3K4me1 in plants, we identified an H3K4me1-specific reader protein, Early heading date 3 (Ehd3), and solved the structure of Ehd3 in complex with the H3K4me1 peptide, revealing a unique binding module differing from the previously reported PHD finger proteins. We further identified an Ehd3-binding protein, SET domain group 724 (SDG724), and the deletion of either Ehd3 or SDG724 caused similar defects in plant phenotype and changes in transcriptome and epigenome profiles. Both Ehd3 and SDG724 are enriched at chromatin regions marked by H3K4me1 but not H3K4me2 or H3K4me3. Ehd3 activates the H3K36 methyltransferase SDG724, and H3K36me2/me3 are colocalized with H3K4me1 in the genomes of land plants. Collectively, our results reveal that H3K4me1 directs the establishment of H3K36me2 and H3K36me3 in land plants.

2025-09-23 | PXD068723 |

ChIP-seq for Ehd3 and SDG724 using HA or GFP antibodies.

Project description:ChIP-seq for Ehd3 and SDG724 using HA or GFP antibodies.

| PRJNA1108699 | ENA

ChIP-seq for Ehd3 and SDG724 using HA or GFP antibodies.

Project description:To investigate the distribution patterns of Ehd3 and SDG724 across the rice genome, we analyzed the data derived from ChIP-seq.

2026-01-26 | GSE266905 | GEO

Transcriptome data (mRNA-seq) for NiP, ehd3-1, sdg724-1, and ehd3 sdg724.

Project description:Transcriptome data (mRNA-seq) for NiP, ehd3-1, sdg724-1, and ehd3 sdg724.

| PRJNA1108705 | ENA

Ehd3 plays an essential role in recruiting SDG724 to H3K4me1-enriched chromatin regions (CUT&Tag).

Project description:We performed CUT&Tag assays to examine SDG724 enrichment in the sdg724 and ehd3 sdg724 mutant backgrounds.

2026-01-26 | GSE311865 | GEO

H3K36me2 ChIP-chip

Project description:Set2p, which mediates histone H3 Lysine 36 dimethylation (H3K36me2) in Saccharomyces cerevisiae, has been shown to associate with RNA polymerase II (RNAP II) at individual loci. Here, ChIP-chip experiments normalized to general nucleosome occupancy reveal that nucleosomes within open reading frames (ORFs) and downstream non-coding chromatin were highly dimethylated at H3K36, and that Set2p activity begins at a stereotypic distance from the initiation of transcription genome-wide. H3K36me2 is scarce in regions upstream of divergently transcribed genes, telomeres, silenced mating loci, and regions transcribed by RNA polymerase III, providing evidence that the enzymatic activity of Set2p is restricted to its association with RNAP II. The presence of H3K36me2 within ORFs correlated with the "on" or "off" state of transcription, but the degree of H3K36 dimethylation within ORFs did not correlate with transcription frequency. This provides evidence that H3K36me2 is established during the initial instances of gene transcription, with subsequent transcription having at most a maintenance role. Accordingly, newly activated genes acquire H3K36me2 in a manner that does not correlate with gene transcript levels. Finally, nucleosomes dimethylated at H3K36 appear to be refractory to loss from highly transcribed chromatin. Thus H3K36me2, which is highly conserved throughout eukaryotic evolution, provides a stable molecular mechanism for establishing chromatin context throughout the genome by distinguishing potential regulatory regions from transcribed chromatin. Keywords: ChIP-chip

2005-10-01 | GSE2991 | GEO

ChIP-seq of histone modifications in rice NiP, ehd3-1, sdg724-1, and ehd3sdg724 using H3, H3K4me1, H3K4me2, H3K4me3, H3K36me1, H3K36me2, and H3K36me3 antibodies

Project description:ChIP-seq of histone modifications in rice NiP, ehd3-1, sdg724-1, and ehd3sdg724 using H3, H3K4me1, H3K4me2, H3K4me3, H3K36me1, H3K36me2, and H3K36me3 antibodies

| PRJNA1108694 | ENA

The H3K36me2 writer-reader dependency in H3K27M-DIPG

Project description:The lysine-to-methionine mutation at residue 27 of histone H3 (H3K27M) is a driving mutation in Diffuse Intrinsic Pontine Glioma (DIPG), a highly aggressive form of pediatric brain tumor with no effective treatment and little chance of survival. H3K27M reshapes the epigenome through a global inhibition of PRC2 catalytic activity, displacement of methylation at lysine 27 of histone H3 (H3K27me2/3), and thus promoting oncogenesis of DIPG. As a consequence, a histone modification H3K36me2, antagonistic to H3K27me2/3, is aberrantly elevated. Here, we investigate the role of H3K36me2 in H3K27M-DIPG by tackling its upstream catalyzing enzymes (writers) and downstream binding factors (readers). We determine that NSD1 and NSD2 are the key writers for H3K36me2. Loss of NSD1/2 in H3K27M-DIPG impedes cellular proliferation in vitro and tumorigenesis in vivo, and disrupts tumor-promoting gene expression programs. Further, we demonstrate that LEDGF and HDGF2 are the main readers that mediate the pro-tumorigenic effects downstream of NSD1/2-H3K36me2. Treatment with a chemically modified peptide mimicking endogenous H3K36me2 dislodges LEDGF/HDGF2 from chromatin and specifically inhibits the proliferation of H3K27M-DIPG. Together, our results indicate a functional pathway of NSD1/2-H3K36me2-LEDGF/HDGF2 as an acquired dependency in H3K27M-DIPG and suggest a possibility to target this pathway for therapeutic interventions.

2021-07-21 | GSE174006 | GEO

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