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LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [ATAC-seq]

ABSTRACT: LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [ATAC-seq]

PROVIDER: PRJNA636661 | ENA |

REPOSITORIES: ENA

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LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1.

Project description:LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1.

| PRJNA636659 | ENA

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [RNA-seq]

Project description:LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [RNA-seq]

| PRJNA636662 | ENA

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [RNA-seq]

Project description:Linker histone H1, the key chromatin structural protein facilitating higher order chromatin folding, isan important epigenetic mark and regulator for gene expression and cellular differentiation. However, mechanisms thatregulate H1 binding affinity to chromatin remain elusive. In an attempt to screen functionallong non-coding RNAs(lncRNAs), we designed a cell-type specific score (CTSS) algorithm on the basis of RNA-seq data derived fromcell lines of different origins, which leads to the identification of an epithelium-specific lncRNA designated assmall nucleolar RNA host gene 8 (SNHG8). In epithelial cells, loss of SNHG8d, a major transcriptof SNHG8, remodels the genomic expression profiletowards differentiation. Mechanistically, SNHG8d is localized in the nucleus and manifests stronginteraction withallthe histone H1 variants detected.Loss of SNHG8dleads to increasedH1 binding affinity to chromatinand subsequentchromatin condensationwhichdictates the epithelial differentiation-orientedgenomic expression remodeling.Further analysis proposes that SNHG8d regulates H1-chromatin affinityby competing with linker DNA forhistone H1 binding througha phase-separation mechanism. Thus, our study revealed a lncRNA-conducted mechanismthat sequesters histone H1 from chromatin through phase separation to sequentially regulatechromatin structure, gene expressionandepithelialdifferentiation.

2021-12-31 | GSE151625 | GEO

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1 [ATAC-seq]

Project description:Linker histone H1, the key chromatin structural protein facilitating higher order chromatin folding, is an important epigenetic mark and regulator for gene expression and cellular differentiation. However, mechanisms thatregulate H1 binding affinity to chromatin remain elusive. In an attempt to screen functionallong non-coding RNAs(lncRNAs), we designed a cell-type specific score (CTSS) algorithm on the basis of RNA-seq data derived fromcell lines of different origins, which leads to the identification of an epithelium-specific lncRNA designated assmall nucleolar RNA host gene 8 (SNHG8). In epithelial cells, loss of SNHG8d, a major transcriptof SNHG8, remodels the genomic expression profiletowards differentiation. Mechanistically, SNHG8d is localized in the nucleus and manifests stronginteraction withallthe histone H1 variants detected.Loss of SNHG8dleads to increasedH1 binding affinity to chromatinand subsequentchromatin condensationwhichdictates the epithelial differentiation-orientedgenomic expression remodeling.Further analysis proposes that SNHG8d regulates H1-chromatin affinityby competing with linker DNA forhistone H1 binding througha phase-separation mechanism. Thus, our study revealed a lncRNA-conducted mechanismthat sequesters histone H1 from chromatin through phase separation to sequentially regulatechromatin structure, gene expressionandepithelialdifferentiation.

2021-12-31 | GSE151624 | GEO

LncRNA SNHG8d impedes chromatin condensation and epithelial differentiation by phase separating histone H1.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-31 | GSE151626 | GEO

Linker histone H1 drives heterochromatin condensation via phase separation in Arabidopsis

Project description:We studied how H1 regulates higher-order chromatin architecture by performing Hi-C. In addition, we tested the effects of H1 domains on nucleosome organisation and DNA methylation by performing MNase-seq and Bisulfite-seq.

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Project description:Chemicals or drugs were demonstrated to accumulate within biomolecule condensates formed through phase separation in cells. Here, we employed super-resolution imaging to search for chemicals that induce phase transition of chromatin at the microscale. We found that adriamycin (doxorubicin), a widely-used chemotherapeutic drug against malignancies, is able to induce local condensation and global conformational change of chromatin in cancer and primary cells. Hi-C and ATAC-seq experiments demonstrated that adriamycin-induced chromatin condensation is accompanied by weakened chromatin interaction within topologically-associated domains, compartment A/B switching, lower chromatin accessibility, and corresponding transcriptomic changes. Mechanistically, adriamycin complexes with histone H1 and induces the phase transition of H1, forming fibrous aggregates in vitro. Our results reveal a new action mechanism of an anti-cancer drug discovered for decades, demonstrate the link between the physical properties of chromatin and gene expression, and suggest that interactions between drugs and biomolecules could exert profound effects on cells.

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