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H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE292289 | GEO | 2025/07/04

REPOSITORIES: GEO

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H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [RNA-Seq]

Project description:In metazoans, nucleosomes harboring H3K79 methylation (H3K79me) deposited by the histone methyltransferase DOT1L decorate actively transcribed genes. Although DOT1L is implicated in transcription regulation and pathogenesis of human diseases such as leukemia and neurological disorders, the role of H3K79me in these biological processes remains elusive. Here, we reveal a novel functional synergism between H3K79me and H3K36 tri-methylation (H3K36me3), another histone modification enriched at active genes, in regulating gene expression and neural cell fate transition. Simultaneous catalytic inactivation of DOT1L and the H3K36 methyltransferase SETD2 via gene editing leads to the global loss of H3K79me and H3K36me3, hyperactive transcription, and failures in neural differentiation. Interestingly, the loss of H3K79me and H3K36me3 causes increased transcription elongation, gained chromatin accessibility at a group of enhancers, and increased binding of TEAD4 transcription factor and its co-activator YAP1 at these enhancers. Furthermore, YAP-TEAD inhibition partially restores the expression levels of hyperactivated genes upon H3K79me/H3K36me3 loss. Taken together, our study demonstrates a synergistic role of H3K79me and H3K36me3 in regulating transcription and cell fate transition, unveils novel mechanisms underlying such synergism, and provides insight into designing therapies that target diseases driven by misregulation or mutations of DOT1L and/or SETD2.

2025-07-04 | GSE292282 | GEO

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ChIP-Seq]

2025-07-04 | GSE292287 | GEO

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ATAC-Seq]

2025-07-04 | GSE292283 | GEO

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells

Project description:H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells

| PRJNA1237820 | ENA

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ChIP-Seq]

Project description:H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ChIP-Seq]

| PRJNA1237827 | ENA

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ATAC-Seq]

Project description:H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [ATAC-Seq]

| PRJNA1237831 | ENA

H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [RNA-Seq]

Project description:H3K79 methylation and H3K36 trimethylation synergistically regulate gene expression in pluripotent stem cells [RNA-Seq]

| PRJNA1237829 | ENA

Dynamic histone H3 methylation during gene induction: HYPB/Setd2 mediates all H3K36 trimethylation.

Project description:Understanding the function of histone modifications across inducible genes in mammalian cells requires quantitative, comparative analysis of their fate during gene activation and identification of enzymes responsible. We produced high-resolution comparative maps of the distribution and dynamics of H3K4me3, H3K36me3, H3K79me2 and H3K9ac across c-fos and c-jun upon gene induction in murine fibroblasts. In unstimulated cells, continuous turnover of H3K9 acetylation occurs on all K4-trimethylated histone H3 tails; distribution of both modifications coincides across promoter and 5' part of the coding region. In contrast, K36- and K79-methylated H3 tails, which are not dynamically acetylated, are restricted to the coding regions of these genes. Upon stimulation, transcription-dependent increases in H3K4 and H3K36 trimethylation are seen across coding regions, peaking at 5' and 3' ends, respectively. Addressing molecular mechanisms involved, we find that Huntingtin-interacting protein HYPB/Setd2 is responsible for virtually all global and transcription-dependent H3K36 trimethylation, but not H3K36-mono- or dimethylation, in these cells. These studies reveal four distinct layers of histone modification across inducible mammalian genes and show that HYPB/Setd2 is responsible for H3K36 trimethylation throughout the mouse nucleus.

| S-EPMC2168397 | biostudies-literature

H3K36 mutations promote sarcomagenesis through genome-wide remodeling of H3K36 and H3K27 methylation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-05-13 | E-GEOD-69291 | biostudies-arrayexpress

H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells.

Project description:During the aging process, bone marrow mesenchymal stem cells (BMSCs) exhibit declined osteogenesis accompanied by excess adipogenesis, which will lead to osteoporosis. Here, we report that the H3 lysine 36 trimethylation (H3K36me3), catalyzed by histone methyltransferase SET-domain-containing 2 (SETD2), regulates lineage commitment of BMSCs. Deletion of Setd2 in mouse bone marrow mesenchymal stem cells (mBMSCs), through conditional Cre expression driven by Prx1 promoter, resulted in bone loss and marrow adiposity. Loss of Setd2 in BMSCs in vitro facilitated differentiation propensity to adipocytes rather than to osteoblasts. Through conjoint analysis of RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) data, we identified a SETD2 functional target gene, Lbp, on which H3K36me3 was enriched, and its expression was affected by Setd2 deficiency. Furthermore, overexpression of lipopolysaccharide-binding protein (LBP) could partially rescue the lack of osteogenesis and enhanced adipogenesis resulting from the absence of Setd2 in BMSCs. Further mechanistic studies demonstrated that the trimethylation level of H3K36 could regulate Lbp transcriptional initiation and elongation. These findings suggest that H3K36me3 mediated by SETD2 could regulate the cell fate of mesenchymal stem cells (MSCs) in vitro and in vivo, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream LBP may represent a potential therapeutic way for new treatment in metabolic bone diseases, such as osteoporosis.

| S-EPMC6233919 | biostudies-literature

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