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RACK7 Senses and Fine-Tunes Enhancer Activity [TT-Seq]

ABSTRACT: Enhancers regulate dynamic gene expression in a spatiotemporal specific manner. A number of positive as well as negative regulators of enhancers have been reported so far. However, whether and how these regulators sense enhancer activity dynamics remains unclear. In this study, we show that a specific enhancer regulator, RACK7, swiftly re-distributes from repressed enhancers to activated enhancers in response to a plethora of acute stimulations. We further show that this process depends on transcription and RACK7 positively regulates enhancer activation by promoting the recruitment of RNA polymerase II. Taken together, our findings suggest that RACK7 senses enhancer activity changes and facilitates their activation during acute stimulations.

ORGANISM(S): Homo sapiens

PROVIDER: GSE282268 | GEO | 2025/07/01

REPOSITORIES: GEO

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RACK7 Senses and Fine-Tunes Enhancer Activity [ChIP-Seq]

Project description:Enhancers regulate dynamic gene expression in a spatiotemporal specific manner. A number of positive as well as negative regulators of enhancers have been reported so far. However, whether and how these regulators sense enhancer activity dynamics remains unclear. In this study, we show that a specific enhancer regulator, RACK7, swiftly re-distributes from repressed enhancers to activated enhancers in response to a plethora of acute stimulations. We further show that this process depends on transcription and RACK7 positively regulates enhancer activation by promoting the recruitment of RNA polymerase II. Taken together, our findings suggest that RACK7 senses enhancer activity changes and facilitates their activation during acute stimulations.

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A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq I)

Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer âbrakeâ to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. ChIP-seq data of RACK7, KDM5C and histone modifications in parental and RACK7-KO ZR-75-30 cells.

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A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq II)

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Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer “brake” to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis.

2016-04-07 | GSE71323 | GEO

A Surveillance System of Active Enhancers by a RACK7-histone Demethylase Complex (ChIP-Seq II)

Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer “brake” to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis.

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