Transient promoter interactions modulate developmental gene activation [ChIPseq]
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ABSTRACT:
PROVIDER: PRJNA1084859 | ENA |
REPOSITORIES: ENA
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Project description:Transient promoter interactions modulate developmental gene activation [CaptureC]
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Project description:Transcriptional induction coincides with the formation of various chromatin topologies, including loss and gain of physical interactions between promoters and distal regulatory elements (DREs). Strong evidence supports that gene activation is accompanied by a general increase in promoter-enhancer interactions. However, it remains unclear how these topological changes are coordinated across time and space to collectively enable transcription. Here we combine chromatin conformation capture with profiling of histone modifications, RNA polymerase II and transcription during an embryonic stem cell differentiation time-course to determine how 3D genome restructuring is related to transcriptional transitions. Using this approach, our data identifies distinct topological alterations that are associated with the magnitude of transcriptional induction. We detect transiently formed interactions between gene promoters and DREs and demonstrate by genetic deletions that these DREs can contribute to the transcriptional induction of associated genes. Finally, by acutely depleting cohesin, we interfere with early transient promoter-enhancer interactions, and show that this impairs the activation of linked genes. Taken together, our study identifies typical topological alterations during gene activation, links them to the magnitude of transcriptional induction, and detects an uncharacterized type of transcriptional enhancers. Our data are compatible with a model where the type of topological pattern that a promoter displays during developmental transitions and the dynamics and magnitude of its transcriptional induction are interdependent.
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Project description:Transient promoter interactions modulate developmental gene activation [RNA-Seq]
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Project description:Transcriptional induction coincides with the formation of various chromatin topologies, including loss and gain of physical interactions between promoters and distal regulatory elements (DREs). Strong evidence supports that gene activation is accompanied by a general increase in promoter-enhancer interactions. However, it remains unclear how these topological changes are coordinated across time and space to collectively enable transcription. Here we combine chromatin conformation capture with profiling of histone modifications, RNA polymerase II and transcription during an embryonic stem cell differentiation time-course to determine how 3D genome restructuring is related to transcriptional transitions. Using this approach, our data identifies distinct topological alterations that are associated with the magnitude of transcriptional induction. We detect transiently formed interactions between gene promoters and DREs and demonstrate by genetic deletions that these DREs can contribute to the transcriptional induction of associated genes. Finally, by acutely depleting cohesin, we interfere with early transient promoter-enhancer interactions, and show that this impairs the activation of linked genes. Taken together, our study identifies typical topological alterations during gene activation, links them to the magnitude of transcriptional induction, and detects an uncharacterized type of transcriptional enhancers. Our data are compatible with a model where the type of topological pattern that a promoter displays during developmental transitions and the dynamics and magnitude of its transcriptional induction are interdependent.
2024-10-29 | GSE261064 | GEO
Project description:Transcriptional induction coincides with the formation of various chromatin topologies, including loss and gain of physical interactions between promoters and enhancers. While strong evidence supports that gene activation is accompanied by a general increase in promoter-enhancer interactions, how these topological changes are coordinated across time and space with other types of interactions to collectively enable gene activation remains unresolved. Here we combine chromatin conformation capture with the profiling of histone modifications and transcription during a finely resolved time-course of embryonic stem cell differentiation to determine how genome restructuring in 3D correlates with and informs transcriptional transitions. Our data indicates that genome restructuring follows only a few common patterns that are related to the magnitude of transcriptional induction. Using this approach we identify transiently formed interactions between gene promoters and distal regulatory elements for which we demonstrate by genetic deletion that they can contribute to the transcriptional induction of associated genes. Finally, using acute depletion of cohesin, we prevent the formation of early promoter-enhancer interactions, and show that this impairs the activation of corresponding genes, compatible with the possibility that early topological changes are instructive for transcription. Taken together, our study identifies the variety of typical topological changes during gene activation, detects an uncharacterized type of transcriptional enhancers and provides evidence that the earliest topological changes can affect the magnitude of gene activation. Our data agrees with the idea that the multitude of topological changes account for appropriate gene induction during cell differentiation.
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Project description:Histone acetylation dynamics modulate chromatin conformation and allele-specific interactions at oncogenic loci (ChIPSeq)
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Project description:In cancer cells, enhancer hijacking mediated by chromosomal alterations and/or increase of histone H3 lysine 27 acetylation (H3K27ac) can support oncogene expression. However, how the chromatin conformation of enhancer-promoter interactions is affected by these events is unclear. Here, by comparing chromatin structure and H3K27ac levels in normal and lymphoma B-cells, we show that enhancer-promoter interacting regions assume different conformations according to the local abundance of H3K27ac. Genetic or pharmacologic depletion of H3K27ac decreases the frequency and the spreading of these interactions, altering oncogene expression. Moreover, enhancer hijacking mediated by chromosomal translocations influences the epigenetic status of the regions flanking the breakpoint, prompting the formation of distinct intra-chromosomal interactions in the two homologous chromosomes. These interactions are accompanied by allele-specific gene expression changes. Overall, our work indicates that H3K27ac dynamics modulate interaction frequency between regulatory regions and can lead to allele-specific chromatin configurations to sustain oncogene expression.
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