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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

ABSTRACT: The emerging 4D genome project aiming to map the dynamics of genomes in spatial and temporal dimension has put forward to developing the mechanisms of how the nucleus is organized and functions. Therefore, processes like cellular senescence characterized by complex events give rise to understanding the regulation network from 1D genome to dynamically organized 3D structure. Unfortunately, how spatial genome reorganization triggers cellular senescence and how it influences senescence-related downstream transcriptional profile remains unaddressed well. Here, we uncover that re re-orchestration of 3D chromatin architecture has occurred in cellular senescence, accompanied with remodeling of enhancer repertories, which in turn facilicate the recruitment of the chromatin reader C/EBPα to newly activated senescence enhancers (SAEs), leading to the expression of SAEs flanking SASP genes kinetics.

ORGANISM(S): Mus musculus

PROVIDER: GSE117209 | GEO | 2018/07/18

REPOSITORIES: GEO

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

Project description:The emerging 4D genome project aiming to map the dynamics of genomes in spatial and temporal dimension has put forward to developing the mechanisms of how the nucleus is organized and functions. Therefore, processes like cellular senescence characterized by complex events give rise to understanding the regulation network from 1D genome to dynamically organized 3D structure. Unfortunately, how spatial genome reorganization triggers cellular senescence and how it influences senescence-related downstream transcriptional profile remains unaddressed well. Here, we uncover that re re-orchestration of 3D chromatin architecture has occurred in cellular senescence, accompanied with remodeling of enhancer repertories, which in turn facilicate the recruitment of the chromatin reader C/EBPα to newly activated senescence enhancers (SAEs), leading to the expression of SAEs flanking SASP genes kinetics.

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