Regulation of neuronal commitment in mouse embryonic stem cells by the Reno/Bahcc1 locus
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ABSTRACT:
PROVIDER: PRJNA512278 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12518100_1.fastq.gz | Fastqsanger.gz | |||
| SRR12518100_2.fastq.gz | Fastqsanger.gz | |||
| SRR12518101_1.fastq.gz | Fastqsanger.gz | |||
| SRR12518101_2.fastq.gz | Fastqsanger.gz | |||
| SRR12518102_1.fastq.gz | Fastqsanger.gz |
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Project description:Regulation of neuronal commitment in mouse embryonic stem cells by the Reno/Bahcc1 locus
2020-09-13 | GSE124517 | GEO
Project description:Mammalian genomes encode thousands of long noncoding RNAs (lncRNAs), yet the biological functions of most of them remain unknown. A particularly rich repertoire of lncRNAs found in mammalian brain and in the early embryo. We used RNA-seq and computational analysis to prioritize lncRNAs that may regulate commitment of pluripotent cells to a neuronal fate and perturbed their expression prior to neuronal differentiation. Knockdown by RNAi of two highly conserved and well-expressed lncRNAs, Reno1 (2810410L24Rik) and lnc-Nr2f1, decreased the expression of neuronal markers and led to massive changes in gene expression in the differentiated cells. We further show that the Reno1 locus forms increasing spatial contacts during neurogenesis with its adjacent protein-coding gene Bahcc1. Loss of either Reno1 or Bahcc1 leads to an early arrest in neuronal commitment, failure to induce a neuronal gene expression program, and to global reduction in chromatin accessibility at regions that are marked by the H3K4me3 chromatin mark at the onset of differentiation. Reno1 and Bahcc1 thus form a previously uncharacterized circuit required for the early steps of neuronal commitment.
| S-EPMC7645239 | biostudies-literature
Project description:Trimethylation of histone H3 lysine 27 (H3K27me3) regulates gene repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module of BAHCC1 (BAHCC1BAH) ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct readout of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by BAHCC1BAH, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is overexpressed in human acute leukemias and interacts with transcriptional co-repressors. In leukemia, depletion of BAHCC1, or disruption of the BAHCC1BAH:H3K27me3 interaction, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to suppression of oncogenesis. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes partial postnatal lethality, supporting a role in development. This study unveils a novel H3K27me3-directed transduction pathway in mammals that relies on a conserved BAH ‘reader’.
2020-11-05 | PXD021679 | Pride
Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
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Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
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Project description:Transcriptional addiction of cancer cells for Super-Enhancer (SE) associated genes has been proven through an extensive use of transcriptional inhibitors against specific co-activators toward which SE are esponentially dependent compared to canonical enhancers. However, each cancer type displays different sensitivity against this new class of drugs whose efficacy may vary according to their transcriptomic profile including the expression of enzymatic proteins able to confer intrinsic tolerance or resistance. Moreover, SE has been observed as well in healthy cells which point a realistic concern toward the specificity of transcriptional inhibitors and their side effects on healthy tissues. Therefore, we looked at SE-associated genes specific for cancer using melanoma as a model. Here, we identified BAHCC1 whose activity is higher in melanoma compare to other cancer types and normal tissues. BAHCC1 is a protein involved both in gene expression and genomic stability. To explore BAHCC1 role in gene expression, we performed functional studies in melanoma cells in basal conditions or upon BAHCC1 silencing. Strikingly, BAHCC1 regulates an E2F-dependent subset of genes together with SWI/SNF chromatin remodelling complex.
2022-04-30 | GSE201702 | GEO
Project description:Tri-methylation of histone H3 lysine 27 (H3K27me3) regulates transcriptional repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module harbored within BAHCC1, a previously uncharacterized chromatin regulator, ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct ‘readout’ of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by the BAH domain, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is significantly overexpressed in human acute leukemia and biochemically, BAHCC1 interacts with repressors SAP30BP and HDAC. In acute leukemia, depletion of BAHCC1, or disruption of the BAHCC1 BAH-mediated ‘readout’ of H3K27me3, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to the suppressed tumor growth. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes postnatal lethality, supporting a role of this pathway in development. Collectively, this study unveils a novel H3K27me3-directed transduction pathway in mammal cells that relies on a conserved BAH ‘reader’, deregulation of which contributes to oncogenesis.
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Project description:Tri-methylation of histone H3 lysine 27 (H3K27me3) regulates transcriptional repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module harbored within BAHCC1, a previously uncharacterized chromatin regulator, ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct ‘readout’ of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by the BAH domain, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is significantly overexpressed in human acute leukemia and biochemically, BAHCC1 interacts with repressors SAP30BP and HDAC. In acute leukemia, depletion of BAHCC1, or disruption of the BAHCC1 BAH-mediated ‘readout’ of H3K27me3, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to the suppressed tumor growth. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes postnatal lethality, supporting a role of this pathway in development. Collectively, this study unveils a novel H3K27me3-directed transduction pathway in mammal cells that relies on a conserved BAH ‘reader’, deregulation of which contributes to oncogenesis.
2020-09-28 | GSE151575 | GEO
Project description:Tri-methylation of histone H3 lysine 27 (H3K27me3) regulates transcriptional repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module harbored within BAHCC1, a previously uncharacterized chromatin regulator, ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct ‘readout’ of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by the BAH domain, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is significantly overexpressed in human acute leukemia and biochemically, BAHCC1 interacts with repressors SAP30BP and HDAC. In acute leukemia, depletion of BAHCC1, or disruption of the BAHCC1 BAH-mediated ‘readout’ of H3K27me3, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to the suppressed tumor growth. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes postnatal lethality, supporting a role of this pathway in development. Collectively, this study unveils a novel H3K27me3-directed transduction pathway in mammal cells that relies on a conserved BAH ‘reader’, deregulation of which contributes to oncogenesis.
2020-09-28 | GSE151574 | GEO
Project description:Tri-methylation of histone H3 lysine 27 (H3K27me3) regulates transcriptional repression, cell-fate determination and differentiation. We report that a conserved Bromo-Adjacent Homology (BAH) module harbored within BAHCC1, a previously uncharacterized chromatin regulator, ‘recognizes’ H3K27me3 specifically and enforces silencing of H3K27me3-demarcated genes in mammalian cells. Biochemical, structural and ChIP-seq-based analyses demonstrate that direct ‘readout’ of H3K27me3 by BAHCC1 is achieved through a hydrophobic trimethyl-lysine-binding ‘cage’ formed by the BAH domain, mediating co-localization of BAHCC1 and H3K27me3-marked genes. BAHCC1 is significantly overexpressed in human acute leukemia and biochemically, BAHCC1 interacts with repressors SAP30BP and HDAC. In acute leukemia, depletion of BAHCC1, or disruption of the BAHCC1 BAH-mediated ‘readout’ of H3K27me3, causes de-repression of H3K27me3-targeted genes that are involved in tumor suppression and cell differentiation, leading to the suppressed tumor growth. In mice, introduction of a germ-line mutation at Bahcc1 to disrupt its H3K27me3 engagement causes postnatal lethality, supporting a role of this pathway in development. Collectively, this study unveils a novel H3K27me3-directed transduction pathway in mammal cells that relies on a conserved BAH ‘reader’, deregulation of which contributes to oncogenesis.
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