Interaction of the pioneer transcription factor GATA3 with nucleosomes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA573080 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10155159_1.fastq.gz | Fastqsanger.gz | |||
| SRR10155159_2.fastq.gz | Fastqsanger.gz | |||
| SRR10155160_1.fastq.gz | Fastqsanger.gz | |||
| SRR10155160_2.fastq.gz | Fastqsanger.gz | |||
| SRR10155161_1.fastq.gz | Fastqsanger.gz |
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Project description:We developed a high-resolution nucleosome mapping method to explore nucleosome positioning around GATA3 binding sites during GATA3-mediated mesenchymal-to-epithelial transition. We found specific correlations between nucleosome positioning and pioneering activities of GATA3.
2020-04-17 | GSE137794 | GEO
Project description:During cellular reprogramming, the pioneer transcription factor GATA3 binds chromatin, and in a context-dependent manner directs local chromatin remodeling and enhancer formation. Here, we use high-resolution nucleosome mapping in human cells to explore the impact of the position of GATA motifs on the surface of nucleosomes on productive enhancer formation, finding productivity correlates with binding sites located near the nucleosomal dyad axis. Biochemical experiments with model nucleosomes demonstrate sufficiently stable transcription factor-nucleosome interaction to empower cryo-electron microscopy structure determination of the complex at 3.15 Å resolution. The GATA3 zinc fingers efficiently bind their target 5'-GAT-3' sequences in the nucleosome when they are located in solvent accessible, consecutive major grooves without significant changes in nucleosome structure. Analysis of genomic loci bound by GATA3 during reprogramming suggests a correlation of recognition motif sequence and spacing that may distinguish productivity of new enhancer formation.
| S-EPMC7434886 | biostudies-literature
Project description:Pioneer transcription factors bind to silent chromatin, and initiate cell fate conversion. One potential pioneer factor, GATA3, is a critical component for multiple cellular programs. GATA3 is of particular interest as it regulates gene expression in breast cancers, and low expression correlates with poor prognosis. Here we demonstrate the pioneering activity of GATA3 utilizing a cellular reprogramming system (the mesenchymal-epithelial transition) in breast cancer cells. During the epithelial transition, GATA3 catalyzes chromatin reprogramming by inducing chromatin opening, active enhancer modifications, and nucleosome remodelling. We determined that the transactivation domain is required for this chromatin reprogramming. Importantly, a mutant lacking the transactivation domain possessed the chromatin binding ability but failed to create open chromatin, suggesting binding alone is not sufficient to induce open chromatin. These data illustrate a fundamental mechanism of GATA3-mediated gene regulation, and provide evidence for a pre-engagement state of closed chromatin bound by a pioneer factor.
2016-01-27 | GSE72141 | GEO
Project description:LFY is pioneer transcription factor
| PRJNA594407 | ENA
Project description:Nuclear DNA is wrapped around core histones to form nucleosomes, which constrains how transcription factors bind to gene regulatory sequences. Pioneer transcription factors have the special ability to bind target DNA on nucleosomes and initiate gene regulatory events, often leading to a local opening of chromatin. Yet the nucleosomal status of such open chromatin, e.g., at active enhancers, is not clear. Here we develop a combination of low and high levels of MNase digestion along with core histone ChIP-seq to assess the presence of nucleosomes at enhancers and promoters in mouse liver. We find that liver-specific enhancers retain preferentially MNase-accessible nucleosomes, with factors bound, substantially more than ubiquitous enhancers. Furthermore, the pioneer factor FoxA2 is required to keep enhancer nucleosomes accessible in chromatin at active liver genes. Thus, nucleosomes are not exclusively repressive to gene regulation when they are retained with, and exposed by, pioneer factors.
2018-05-30 | GSE71947 | GEO
Project description:Nuclear DNA is wrapped around core histones to form nucleosomes, which constrains how transcription factors bind to gene regulatory sequences. Pioneer transcription factors have the special ability to bind target DNA on nucleosomes and initiate gene regulatory events, often leading to a local opening of chromatin. Yet the nucleosomal configuration of such open chromatin and the basis for chromatin opening is unclear. Here we combine low and high levels of MNase digestion along with core histone ChIP-seq to assess the presence of nucleosomes at enhancers and promoters in mouse liver. We find that the pioneer factor FoxA displaces linker histone H1, thereby keeping enhancer nucleosomes accessible in chromatin and helping other transcription factors bind. MNase-accessible nucleosomes, bound by transcription factors, are retained substantially more at liver-specific enhancers than promoters and tissue-ubiquitous enhancers. Thus, nucleosomes are not exclusively repressive to gene regulation when they are retained with, and exposed by, pioneer factors.
2016-04-08 | GSE77670 | GEO
Project description:Though the in vitro structural and in vivo spatial characteristics of transcription factor (TF) binding are well defined, TF interactions with chromatin and other companion TFs during development are poorly understood. To analyze such interactions in vivo, we profiled several TFs across a time course of human embryonic stem cell differentiation via CUT&RUN epigenome profiling, and studied their interactions with nucleosomes and co-occurring TFs by Enhanced Chromatin Occupancy (EChO), a computational strategy for classifying TF binding characteristics across time and space. EChO shows that at different enhancer targets, the same TF can employ either direct DNA binding, or “pioneer” nucleosome binding to access them. Pioneer binding is correlated with local binding of other TFs and enhancer motif character, including degeneracy at key bases in the pioneer factor target motif. Our strategy reveals a dynamic exchange of TFs at enhancers across developmental time that is aided by pioneer nucleosome binding.
2019-06-25 | GSE128499 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE28006: The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [mRNA profiling] GSE28007: The pioneer factor PBX1 guides a distinct ERa signaling in breast cancer [ChIP-seq] Refer to individual Series
2011-09-29 | E-GEOD-28008 | biostudies-arrayexpress
Project description:The nucleosome is a fundamental unit of chromatin in eukaryotes, and generally prevents the binding of transcription factors to genomic DNA. Pioneer transcription factors overcome the nucleosome barrier, and bind their target DNA sequences in chromatin. OCT4 is a representative pioneer transcription factor that plays a role in stem cell pluripotency. In the present study, we biochemically analyzed the nucleosome binding by OCT4. Crosslinking mass spectrometry showed that OCT4 binds the nucleosome.
2020-05-13 | PXD019160 | JPOST Repository
Project description:Background: The androgen receptor (AR) is a tumor suppressor in estrogen receptor (ER) positive breast cancer, a role sustained in some ER negative breast cancers. Key factors dictating AR genomic activity in a breast context are largely unknown. Herein, we employed an unbiased chromatin immunoprecipitation-based proteomic technique to identify endogenous AR interacting co-regulatory proteins in ER positive and negative models of breast cancer to gain new insight into mechanisms of AR signaling in this disease. Results: The DNA-binding factor GATA3 is identified and validated as a novel AR interacting protein in breast cancer cells irrespective of ER status. AR activation by the natural ligand 5α-dihydrotestosterone (DHT) increases nuclear AR-GATA3 interactions, resulting in AR-dependent enrichment of GATA3 chromatin binding at a sub-set of genomic loci. Silencing GATA3 reduces but does not prevent AR DNA binding and transactivation of genes associated with AR/GATA3 co-occupied loci, indicating a co-regulatory role for GATA3 in AR signaling. DHT-induced AR/GATA3 binding coincides with upregulation of luminal differentiation genes, including EHF and KDM4B, established master regulators of a breast epithelial cell lineage. These findings are validated in a patient-derived xenograft model of breast cancer. Interaction between AR and GATA3 is also associated with AR-mediated growth inhibition in ER positive and ER negative breast cancer.
2024-01-30 | PXD047997 | Pride