Genome-wide chromatin interactions identify characteristic promoter-distal loops
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ABSTRACT:
PROVIDER: PRJNA528483 | ENA |
REPOSITORIES: ENA
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Project description:We developed a novel computational model, HiSIF (Hi-C Significant Interacting Fragments), which uses a Poisson Mixture Model (PMM) with a power-law decay background. We compared its performance to some existing programs with publicly available Hi-C data, and then applied it to in situ Hi-C data in breast cancer sensitive and resistant cells.
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Project description:Interactions between transcriptional promoters and their distal regulatory elements play an important role in transcriptional regulation; however, the extent to which these interactions are subject to rapid modulations in response to signals is unknown. Here, we use promoter capture Hi-C to demonstrate a rapid reorganization of promoter anchored chromatin loops within four hours after induction of differentiation of 3T3-L1 preadipocytes. This reorganization is tightly coupled to dynamic changes in target gene expression. The formation of promoter-enhancer loops is tightly linked to the activation of poised (histone H3 lysine 4 mono- and dimethylated) enhancers, as evidenced by the acquisition of histone H3 lysine 27 acetylation and the binding of MED1, SMC1 and P300 proteins to these regions. Intriguingly, formation of loops connecting activated enhancers and promoters is also associated with extensive recruitment of corepressors such as NCoR and HDACs, indicating that this class of coregulators may play a previously unrecognized role during enhancer activation.
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Project description:Current computational methods on Hi-C analysis focused on identifying Mb-size domains often failed to unveil the underlying functional and mechanistic relationship of chromatin structure and gene regulation. We developed a novel computational method HiSIF to identify genome-wide interacting loci. We illustrated HiSIF outperformed other tools for identifying chromatin loops. We applied it to Hi-C data in breast cancer cells and identified 21 genes with gained loops showing worse relapse-free survival in endocrine-treated patients, suggesting the genes with enhanced loops can be used for prognostic signatures for measuring the outcome of the endocrine treatment. HiSIF is available at https://github.com/yufanzhouonline/HiSIF .
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Project description:R-loops are features of chromatin consisting of a strand of DNA hybridized to RNA, as well as the expelled complementary DNA strand. R-loops are enriched at promoters where they have recently been shown to have important roles in modifying gene expression. However, the location of promoter-associated R-loops and the genomic domains they perturb to modify gene expression remain unclear. To resolve this issue, we developed a bisulfite-based approach, bisDRIP-seq, to map R-loops across the genome at near-nucleotide resolution in MCF-7 cells. We found the location of promoter-associated R-loops is dependent on the presence of introns. In intron-containing genes, R-loops are bounded between the transcription start site and the first exon-intron junction. In intronless genes, the 3' boundary displays gene-specific heterogeneity. Moreover, intronless genes are often associated with promoter-associated R-loop formation. Together, these studies provide a high-resolution map of R-loops and identify gene structure as a critical determinant of R-loop formation.
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Project description:The CCCTC-binding factor (CTCF) is widely regarded as a key player in chromosome organization in mammalian cells, yet direct assessment of its role in genome architecture and gene regulation has been difficult. Here, we use auxin-inducible degron techniques to acutely deplete CTCF to determine how loss of CTCF affect chromatin organization and gene expression. In mouse embryonic stem cells, depletion of CTCF results in rapid loss of chromatin loops anchored at CTCF-binding sites without major disruption to chromatin compartments and topological domains. In the absence of CTCF, many lineage-specific genes fail to express properly during differentiation to neural precursor cells, but transcriptional regulation of most genes is unaffected. Genes dependent on CTCF for induction are generally bound by the factor at promoters, which are connected to distal enhancers via CTCF-dependent chromatin loops. By contrast, CTCF-independent genes generally lack CTCF binding at the promoter and are generally closer to enhancers. These results refine our understanding of CTCF function in chromatin organization and gene regulation.
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Project description:The CCCTC-binding factor (CTCF) is widely regarded as a key player in chromosome organization in mammalian cells, yet direct assessment of its role in genome architecture and gene regulation has been difficult. Here, we use auxin-inducible degron techniques to acutely deplete CTCF to determine how loss of CTCF affect chromatin organization and gene expression. In mouse embryonic stem cells, depletion of CTCF results in rapid loss of chromatin loops anchored at CTCF-binding sites without major disruption to chromatin compartments and topological domains. In the absence of CTCF, many lineage-specific genes fail to express properly during differentiation to neural precursor cells, but transcriptional regulation of most genes is unaffected. Genes dependent on CTCF for induction are generally bound by the factor at promoters, which are connected to distal enhancers via CTCF-dependent chromatin loops. By contrast, CTCF-independent genes generally lack CTCF binding at the promoter and are generally closer to enhancers. These results refine our understanding of CTCF function in chromatin organization and gene regulation.
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Project description:The CCCTC-binding factor (CTCF) is widely regarded as a key player in chromosome organization in mammalian cells, yet direct assessment of its role in genome architecture and gene regulation has been difficult. Here, we use auxin-inducible degron techniques to acutely deplete CTCF to determine how loss of CTCF affect chromatin organization and gene expression. In mouse embryonic stem cells, depletion of CTCF results in rapid loss of chromatin loops anchored at CTCF-binding sites without major disruption to chromatin compartments and topological domains. In the absence of CTCF, many lineage-specific genes fail to express properly during differentiation to neural precursor cells, but transcriptional regulation of most genes is unaffected. Genes dependent on CTCF for induction are generally bound by the factor at promoters, which are connected to distal enhancers via CTCF-dependent chromatin loops. By contrast, CTCF-independent genes generally lack CTCF binding at the promoter and are generally closer to enhancers. These results refine our understanding of CTCF function in chromatin organization and gene regulation.
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Project description:The CCCTC-binding factor (CTCF) is widely regarded as a key player in chromosome organization in mammalian cells, yet direct assessment of its role in genome architecture and gene regulation has been difficult. Here, we use auxin-inducible degron techniques to acutely deplete CTCF to determine how loss of CTCF affect chromatin organization and gene expression. In mouse embryonic stem cells, depletion of CTCF results in rapid loss of chromatin loops anchored at CTCF-binding sites without major disruption to chromatin compartments and topological domains. In the absence of CTCF, many lineage-specific genes fail to express properly during differentiation to neural precursor cells, but transcriptional regulation of most genes is unaffected. Genes dependent on CTCF for induction are generally bound by the factor at promoters, which are connected to distal enhancers via CTCF-dependent chromatin loops. By contrast, CTCF-independent genes generally lack CTCF binding at the promoter and are generally closer to enhancers. These results refine our understanding of CTCF function in chromatin organization and gene regulation.
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