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Genome-wide maps of histone PTMs and co-factors in pluripotent mouse embryonic stem cells (mESCs) and epiblast-like cells (EpiLCs)

ABSTRACT: We report here the genome wide mapping of histone PTMs and chromatin bound factors in pluripotent control and H3K27R base edited mouse embryonic stem cells (mESCs) and epiblast-like cells (EpiLCs) using ChIP-Seq technology. We have deposited results from chromatin immunoprecipitations done using antibodies against Rpb1 (Pol-II), Med1,H3.3, H3K27me1, H3K27me2, H3K27me3 and H3K27ac (rabbit and mouse monoclonal antibodies). We show the loss of all H3K27 from H3.1/2/3 results in loss of associated K27 methylation and acetylation as expected. In such cells, there are only modest changes to MED1 or RNA Pol-II binding or activity that correlate with transcriptional status, suggesting that H3K27ac is not required to initiate or maintain transcription of genes, while loss of H3K27me3 associates with derepression of Polycomb target genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE160974 | GEO | 2021/12/06

REPOSITORIES: GEO

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De novo heterozygous variants in POLR2A cause a neurodevelopmental syndrome with infantile-onset hypotonia

Project description: ABSTRACT POLR2A encodes RPB1, the largest subunit of the RNA polymerase II (pol II) complex, which is responsible for transcription of all ~21,000 protein-encoding genes. Here we describe the first fifteen patients harboring de novo heterozygous variants in POLR2A. The majority presents with profound infantile onset hypotonia and developmental delay. Missense variants that were expected to exert only mild structural effects, lead to malfunctioning RPB1, thereby inducing a dominant negative effect on pol II function. Intriguingly, these patients presented with a severe clinical phenotype. Conversely, variants expected to result in loss-of-function, leading to reduced availability of RPB1 were better tolerated: these patients exhibited the mildest phenotypes.

2019-09-02 | PXD011355 | Pride

EGAS00001003953-ChIPseq - samples

Project description:ChIPseq data for human glioblastoma patients, EGAS00001003953. Mix of input, H3K27ac, H3K27me1, H3K27me3, H3K36me3, H3K4me1, H3K4me3, H3K9me3 and BRD, 20 human samples, 2 cell lines (LN229, ZH487).

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AMPKα2 binds to chromatin to regulate gene expression in ALL cells [ChIP-seq]

Project description:To identify genome-wide genes regulated by direct association of AMPKα2 to chromatin, ChIP-Seq assays were performed using HA (HA-AMPKα2) and RPB1 (RNA Pol II) antibodies in CCRF-CEM/HA-AMPKα2 (CN2) cells treated with glucose deprivation or no treatment controls. ChIP-seq analysis identified around 600 genes to which loci AMPKα2 was directly bound; many of these genes with HA-AMPKα2 recruitment overlapped with genes exhibiting RNA Pol II enrichment.

2023-12-06 | GSE210213 | GEO

Genome-wide map of 4 histone modifications and PolII in iPSC-derived human cardiomyocytes

Project description:We generated maps of H3K4me1, H3K27ac (enhancers), H3K4me3, Pol II (promoters) and H3K27me3 (repressed chromatin) in the genome of human iPSC-derived cardiomyocytes Differentiation of cardiomyocytes from iPSC followed by ChIP-seq of H3K27ac, H34me1, H327me3, H3K4me3 and PolII

2016-02-22 | E-GEOD-77267 | biostudies-arrayexpress

ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

2021-05-05 | GSE131710 | GEO

RPB1 ChIP-Seq of adrenal glands tissue from Wild Type (WT) and Armc5 knockout mice

Project description:RPB1-specific ubiquitin ligase (E3) controls the degradation of this largest subunit of Pol II and consequently the Pol II pool size. Although several RPB1-specific E3s have been documented, their function is only revealed in cells with massive DNA damage. We demonstrated that ARMC5 physically interacted with cullin3 (CUL3) and RPB1. ARMC5 is an armadillo domain-containing protein with unknown mechanisms of action. ARMC5 deletion caused significant RPB1 accumulation in all the major organs under a physiological condition in the absence of artificially induced DNA damage. This is accompanied by reduced RPB1 ubiquitination. In vitro ubiquitination assay proved that ARMC5, CUL3, and RBX1 formed an effective E3 for RPB1. RPB1 was confirmed as being highly accumulated in the adrenal gland nodules from PBMAH patients with mutations in the ARMC5 coding sequence. Surprisingly, the compromised RPB1 degradation did not lead to increased Pol II stalling according to ChIP-Seq, or a general decrease of gene transcription according to RNA-seq. On the contrary, among 1486 differentially expressed genes in the KO adrenal glands, 93.5% of them were upregulated, probably due to the enlarged Pol II pool size. Our results showed that the ARMC3-CUL3 E3 was the dominant E3 in normal cells and organs and controlled Pol II pool size. The abnormally large Pol II pool size due to ARMC5 mutation dysregulated a large number of genes that in turn led to many phenotypes, including PBMAH in humans.

2022-05-20 | GSE169578 | GEO

RNA-Seq of adrenal glands tissue from Wild Type (WT) and Armc5 knockout mice

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Establishment of a novel in vitro transcription assay

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2021-11-03 | PXD017881 | Pride

SPT5 stabilizes promoter-proximal RNA polymerase II prior to release into gene bodies

Project description:The regulation of gene expression by RNA polymerase II (Pol II) is a multistep process requiring the concerted action of diverse transcription factors. Very little is known about in vivo function of transcription factor SPT5 as its deletion results in loss of viability. To circumvent this issue and define in vivo mechanism of action for SPT5, we employed acute degradation of SPT5 and studied its consequence on transcription. We find that SPT5 loss triggers degradation of the core Pol II subunit RPB1, a process which we show to be evolutionarily conserved from yeast to human. This RPB1 degradation requires the E3 ubiquitin ligase Cullin 3, the unfoldase VCP/p97 and a novel form of CDK9 kinase complex. SPT5 specifically stabilizes Pol II at promoter proximal regions, permitting Pol II release from promoters to gene bodies. Our findings provide mechanistic insight into the in vivo function of SPT5 in stabilization of promoter-proximal Pol II prior to release into gene bodies for safeguarding accurate gene expression.

2021-08-31 | GSE168827 | GEO

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2012-11-30 | E-GEOD-42161 | biostudies-arrayexpress

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