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Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

ABSTRACT: Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

PROVIDER: PRJNA136591 | ENA |

REPOSITORIES: ENA

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Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [expression]

Project description:Genome wide gene expression profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The sample treated with non target siRNA and PBS serves as control sample. Total RNA obtained from isolated RKO cells.

2013-01-01 | E-GEOD-26684 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [Methylation]

Project description:Genome wide DNA methylation profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The Illumina Infinium 27k Human DNA methylation Beadchip v1.2 was used to obtain DNA methylation profiles across 27,578 CpGs in treated RKO cells. Samples included cells under 4 different treatments. The sample treated with non target siRNA and PBS serves as control sample. Bisulphite converted DNA from the 4 samples were hybridised to the Illumina Infinium 27k Human Methylation Beadchip v1.2

2013-01-01 | E-GEOD-26433 | biostudies-arrayexpress

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [expression]

2013-01-01 | GSE26684 | GEO

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange [Methylation]

2013-01-01 | GSE26433 | GEO

Mechanistic basis of gene regulation by SRCAP and H2A.Z

Project description:A central problem in gene regulation is to discriminate gene regulatory functions of chromatin composition from the one of chromatin-modifying complexes. This question has been virtually unexplored in the context of the H2A.Z histone variant and its incorporation into nucleosomes by the Snf2 Related CREBBP Activator Protein (SRCAP) complex. Here we combine rapid SRCAP depletion, a SRCAP mutant lacking H2A.Z deposition activity, and quantitative genome-wide approaches to dissect how SRCAP and H2A.Z regulate transcription in pluripotent stem cells. We find that SRCAP exhibits essential H2A.Z-independent functions in preventing DNA binding of lineage-specific transcription factors at enhancers and stimulating transcription factor binding at promoters. In contrast, H2A.Z acts mainly as a transcriptional repressor that requires dynamic reloading by SRCAP throughout the cell cycle. Our study demonstrates how the SRCAP-H2A.Z axis broadly orchestrates transcription to promote self-renewal, inhibit differentiation, and maintain plasticity of pluripotent stem cells.

2026-01-05 | PXD052934 | Pride

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-01-01 | E-GEOD-26685 | biostudies-arrayexpress

Structural insights into histone exchange by human SRCAP complex

Project description:Histone variant H2A.Z is found at promoters and regulates transcription. The ATP-dependent chromatin remodeler SRCAP complex (SRCAP-C) promotes the replacement of canonical histone H2A-H2B dimer with H2A.Z-H2B dimer. Here, we determined structures of human SRCAP-C bound to H2A-containing nucleosome at near-atomic resolution. The SRCAP subunit integrates a 6-subunit actin-related protein (ARP) module and an ATPase-containing motor module. The ATPase-associated ARP module encircles half of the nucleosome along the DNA and may restrain net DNA translocation, a unique feature of SRCAP-C. The motor module adopts distinct nucleosome-binding modes in the apo (nucleotide-free), ADP-bound, and ADP-BeFx-bound states, suggesting that ATPase-driven movement destabilizes H2A-H2B by unwrapping the entry DNA and pulls H2A-H2B out of nucleosome through the ZNHIT1 subunit. Structure-guided chromatin immunoprecipitation (ChIP) sequencing analysis confirmed the requirement of H2A-contacting ZNHIT1 in maintaining H2A.Z occupancy on the genome. Our study provides structural insights into the mechanism of H2A-H2A.Z exchange mediated by SRCAP-C.

2024-02-10 | GSE249825 | GEO

Coordinated Chromatin Remodeling induced by Demethylation requires SRCAP mediated H2A.Z exchange

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

2013-01-01 | GSE26685 | GEO

Mechanistic basis of gene regulation by SRCAP and H2A.Z (ChIP-Seq)

Project description:A central problem in gene regulation is to discriminate gene regulatory functions of chromatin composition from the one of chromatin-modifying complexes. This question has been virtually unexplored in the context of the H2A.Z histone variant and its incorporation into nucleosomes by the Snf2 Related CREBBP Activator Protein (SRCAP) complex. Here we combine rapid SRCAP depletion, a SRCAP mutant lacking H2A.Z deposition activity, and quantitative genome-wide approaches to dissect how SRCAP and H2A.Z regulate transcription in pluripotent stem cells. We find that SRCAP exhibits essential H2A.Z-independent functions in preventing DNA binding of lineage-specific transcription factors at enhancers and stimulating transcription factor binding at promoters. In contrast, H2A.Z acts mainly as a transcriptional repressor that requires dynamic reloading by SRCAP throughout the cell cycle. Our study clarifies how the SRCAP-H2A.Z axis broadly orchestrates transcription to promote self-renewal, inhibit differentiation, and maintain plasticity of pluripotent stem cells.

2026-01-06 | GSE269304 | GEO

Mechanistic basis of gene regulation by SRCAP and H2A.Z (ATAC-Seq)

Project description:A central problem in gene regulation is to discriminate gene regulatory functions of chromatin composition from the one of chromatin-modifying complexes. This question has been virtually unexplored in the context of the H2A.Z histone variant and its incorporation into nucleosomes by the Snf2 Related CREBBP Activator Protein (SRCAP) complex. Here we combine rapid SRCAP depletion, a SRCAP mutant lacking H2A.Z deposition activity, and quantitative genome-wide approaches to dissect how SRCAP and H2A.Z regulate transcription in pluripotent stem cells. We find that SRCAP exhibits essential H2A.Z-independent functions in preventing DNA binding of lineage-specific transcription factors at enhancers and stimulating transcription factor binding at promoters. In contrast, H2A.Z acts mainly as a transcriptional repressor that requires dynamic reloading by SRCAP throughout the cell cycle. Our study clarifies how the SRCAP-H2A.Z axis broadly orchestrates transcription to promote self-renewal, inhibit differentiation, and maintain plasticity of pluripotent stem cells.

2026-01-06 | GSE269302 | GEO

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