Reciprocal regulation of phosphatidylcholine synthesis and H3K36 methylation programs metabolic adaptation
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ABSTRACT:
PROVIDER: PRJNA752757 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15365257_1.fastq.gz | Fastqsanger.gz | |||
| SRR15365257_2.fastq.gz | Fastqsanger.gz | |||
| SRR15365258_1.fastq.gz | Fastqsanger.gz | |||
| SRR15365258_2.fastq.gz | Fastqsanger.gz | |||
| SRR15365259_1.fastq.gz | Fastqsanger.gz |
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Project description:Reciprocal regulation of phosphatidylcholine synthesis and H3K36 methylation programs metabolic adaptation II
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Project description:While epigenetic regulation in early development and differentiation is relatively well-characterized, the precise mechanisms that subsequently maintain specialized cell states remain largely unexplored. Here, we employed histone H3.3 mutants to uncover a crucial role for H3K36 methylation in the maintenance of cell identities across diverse developmental contexts. Focusing on the experimentally induced conversion of fibroblasts to pluripotent stem cells, we show that H3K36M-mediated disruption of H3K36 methylation endowed reprogramming intermediates with a plastic state poised to acquire pluripotency in virtually every cell. At a cellular level, H3K36M rendered mesenchymal cells insensitive to TGF signals and thus facilitated epithelial plasticity. At a molecular level, H3K36M led to the downregulation of mesenchymal genes by depleting H3K36me2 and H3K27ac at associated enhancers. In parallel, H3K36M led to the upregulation of epithelial and stem cell genes by enabling enhancer accessibility and hypomethylation. Mechanistically, we found that Tet-dependent demethylation uncouples pluripotency enhancer activation from somatic enhancer decommissioning in K36M cells. This dynamic switch of enhancer activities redirects Sox2 binding from promiscuous somatic targets to bona fide stem cell targets crucial for the establishment of the pluripotency network. Together, our findings reveal a dual role for H3K36 methylation in the maintenance of cell identity, by integrating a key developmental pathway into sustained expression of cell type-specific programs, and by opposing the expression of alternative lineage programs through continual enhancer methylation. Our results provide crucial insight into the impact of dynamic H3K36 methylation patterns on physiological and pathological cell fate transitions, including development, tissue regeneration and cancer.
2023-02-20 | GSE203606 | GEO
Project description:While epigenetic regulation in early development and differentiation is relatively well-characterized, the precise mechanisms that subsequently maintain specialized cell states remain largely unexplored. Here, we employed histone H3.3 mutants to uncover a crucial role for H3K36 methylation in the maintenance of cell identities across diverse developmental contexts. Focusing on the experimentally induced conversion of fibroblasts to pluripotent stem cells, we show that H3K36M-mediated disruption of H3K36 methylation endowed reprogramming intermediates with a plastic state poised to acquire pluripotency in nearly all cells. At a cellular level, H3K36M rendered mesenchymal cells insensitive to TGF signals and thus facilitated epithelial plasticity. At a molecular level, H3K36M led to the downregulation of mesenchymal genes by depleting H3K36me2 and H3K27ac at associated enhancers. In parallel, H3K36M led to the upregulation of epithelial and stem cell genes by enabling enhancer accessibility and hypomethylation. Mechanistically, we found that Tet-dependent demethylation uncouples pluripotency enhancer activation from somatic enhancer decommissioning in K36M cells. This dynamic switch of enhancer activities redirects Sox2 binding from promiscuous somatic targets to bona fide stem cell targets crucial for the establishment of the pluripotency network. Together, our findings reveal a dual role for H3K36 methylation in the maintenance of cell identity by integrating a key developmental pathway into sustained expression of cell type-specific programs, and by opposing the expression of alternative lineage programs through continual enhancer methylation. Our results provide crucial insight into the impact of dynamic H3K36 methylation patterns on physiological and pathological cell fate transitions, including development, tissue regeneration and cancer.
2023-02-04 | GSE203536 | GEO
Project description:In budding yeast, Set2 catalyzes di- and trimethylation of H3K36 (H3K36me2 and H3K36me3) via an interaction between its SRI domain and C-terminal repeats of RNA polymerase II (Pol2) phosphorylated at Ser2 and Ser5 (CTD-S2,5-P). H3K36me2 recruits the Rpd3S histone deacetylase complex to repress cryptic transcription from transcribed regions. In fission yeast, Set2 is also responsible for H3K36 methylation, which represses a subset of RNAs including heterochromatic and subtelomeric RNAs, at least in part via recruitment of Clr6 complex II, a homolog of Rpd3S. Here, we show that CTD-S2Pâdependent interaction of fission yeast Set2 with Pol2 via the SRI domain is required for formation of H3K36me3, but not H3K36me2. H3K36me3 silenced heterochromatic and subtelomeric transcripts through post-transcriptional and transcriptional mechanisms, respectively, whereas H3K36me2 did not. Clr6 complex II appeared not to be responsible for heterochromatic silencing. Our results demonstrate that H3K36 methylation has multiple outputs in fission yeast; these findings provide insight into the multiple roles of H3K36 methylation in metazoans, which have different enzymes for synthesis of H3K36me1/2 and H3K36me3. Gene expression profile at exponentially-growing phase.in the fission yeast deletion mutants of set2.
2016-02-04 | E-GEOD-66821 | biostudies-arrayexpress
Project description:While epigenetic regulation in early development and differentiation is relatively well-characterized, the precise mechanisms that subsequently maintain specialized cell states remain largely unexplored. Here, we employed histone H3.3 mutants to uncover a crucial role for H3K36 methylation in the maintenance of cell identities across diverse developmental contexts. Focusing on the experimentally induced conversion of fibroblasts to pluripotent stem cells, we show that H3K36M-mediated disruption of H3K36 methylation endowed reprogramming intermediates with a plastic state poised to acquire pluripotency in virtually every cell. At a cellular level, H3K36M rendered mesenchymal cells insensitive to TGF signals and thus facilitated epithelial plasticity. At a molecular level, H3K36M led to the downregulation of mesenchymal genes by depleting H3K36me2 and H3K27ac at associated enhancers. In parallel, H3K36M led to the upregulation of epithelial and stem cell genes by enabling enhancer accessibility and hypomethylation. Mechanistically, we found that Tet-dependent demethylation uncouples pluripotency enhancer activation from somatic enhancer decommissioning in K36M cells. This dynamic switch of enhancer activities redirects Sox2 binding from promiscuous somatic targets to bona fide stem cell targets crucial for the establishment of the pluripotency network. Together, our findings reveal a dual role for H3K36 methylation in the maintenance of cell identity, by integrating a key developmental pathway into sustained expression of cell type-specific programs, and by opposing the expression of alternative lineage programs through continual enhancer methylation. Our results provide crucial insight into the impact of dynamic H3K36 methylation patterns on physiological and pathological cell fate transitions, including development, tissue regeneration and cancer.
2023-02-21 | GSE203491 | GEO
Project description:While epigenetic regulation in early development and differentiation is relatively well-characterized, the precise mechanisms that subsequently maintain specialized cell states remain largely unexplored. Here, we employed histone H3.3 mutants to uncover a crucial role for H3K36 methylation in the maintenance of cell identities across diverse developmental contexts. Focusing on the experimentally induced conversion of fibroblasts to pluripotent stem cells, we show that H3K36M-mediated disruption of H3K36 methylation endowed reprogramming intermediates with a plastic state poised to acquire pluripotency in virtually every cell. At a cellular level, H3K36M rendered mesenchymal cells insensitive to TGF signals and thus facilitated epithelial plasticity. At a molecular level, H3K36M led to the downregulation of mesenchymal genes by depleting H3K36me2 and H3K27ac at associated enhancers. In parallel, H3K36M led to the upregulation of epithelial and stem cell genes by enabling enhancer accessibility and hypomethylation. Mechanistically, we found that Tet-dependent demethylation uncouples pluripotency enhancer activation from somatic enhancer decommissioning in K36M cells. This dynamic switch of enhancer activities redirects Sox2 binding from promiscuous somatic targets to bona fide stem cell targets crucial for the establishment of the pluripotency network. Together, our findings reveal a dual role for H3K36 methylation in the maintenance of cell identity, by integrating a key developmental pathway into sustained expression of cell type-specific programs, and by opposing the expression of alternative lineage programs through continual enhancer methylation. Our results provide crucial insight into the impact of dynamic H3K36 methylation patterns on physiological and pathological cell fate transitions, including development, tissue regeneration and cancer.
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