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Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

ABSTRACT: The goal of these ATAC-seq experiments was to determine changes in chromatin accesiblity caused by loss of Gibbin (AHDC1) or GATA3 in non-neural ectoderm.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163769 | GEO | 2022/02/13

REPOSITORIES: GEO

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Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

Project description:Gibbin drives epithelial development by toggling CTCF binding and DNA methylation

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The Xia-Gibbs Syndrome protein Gibbin regulates mesodermal DNA methylation to pattern epithelial development (RNA-Seq)

Project description:The goal of these RNA-seq experiments was to determine changes in gene expression caused by loss of Gibbin (AHDC1) or GATA3 at various time points following addition of RA/BMP4.

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DNA binding site for TFAP2A in non-neural ectoderm

Project description:The objective of this experiment was to determine the DNA binding site for TFAP2A in non-neural ectoderm.

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Identification of transcriptome of mouse non-neural ectoderm during nueral tube closure and gene enrichment compared to remaining neural tube tissue

Project description:The process of neural tube closure is a highly complex morphogenetic event that results in the generation of the primordial central nervous system. During formation of the neural tube, the non-neural ectoderm separates from the neighboring neural ectoderm and forms a single layer epithelial sheet that overlies the closed neural tube. Previous work has shown that the non-neural ectoderm is necessary for proper cranial neural tube closure, however little is known about this cell population at the molecular level or how the non-neural ectoderm contributes to neural tube closure. In this study, we used a mouse genetic system to fluorescently label the non-neural ectoderm cells and FACS sorted these cells away from the other cell populations in the neural tube. We performed high throughput RNA-sequencing to identify the transcriptome of the non-neural ectoderm and compared the gene expression profile of non-neural ectoderm cells to the remaining population of cells within the neural tube in order to identify which genes are enriched within the non-neural ectoderm. This analysis provides a clue as to which underlying molecular processes may be important for non-neural ectoderm function during neural tube closure.

2016-04-27 | GSE72059 | GEO

Accumulation of CTCF-binding sites drives expression divergence between tandemly duplicated genes in humans.

Project description:BACKGROUND: During eukaryotic genome evolution, tandem gene duplication is the most frequent event giving rise to clustered gene families. However, how expression divergence between tandemly duplicated genes has emerged and maintained remain unclear. In particular, it is unknown if epigenetic regulators have been involved in the process. RESULTS: We demonstrate that CCCTC-binding factor (CTCF), the master epigenetic regulator and the only known insulator protein in humans, has played a predominant role in generating divergence in both expression profiles and expression levels between adjacent paralogs in the human genome. This phenomenon was not observed for non-paralogous adjacent genes. After tandem duplication events, CTCF-binding sites gradually accumulate between paralogs. This trend was more prominent for genes involved in particular functions. CONCLUSIONS: The accumulation of CTCF-binding sites drives expression divergence of tandemly duplicated genes. This process is likely targeted by natural selection. Our study reveals the importance of CTCF to the evolution of animal diversity and complexity.

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RPL35A drives ovarian cancer progression by promoting the binding of YY1 to CTCF promoter

Project description: Not available

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The¬¬¬ androgen receptor interacts with GATA3 to transcriptionally regulate a luminal epithelial cell phenotype in breast cancer

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

CTCF binding polarity determines chromatin looping [ChIP-seq]

Project description:CTCF binding polarity determines chromatin looping CTCF ChIPseq was performed in E14 embryonic stem cells and neural precursor cells

2015-10-29 | E-GEOD-71158 | biostudies-arrayexpress

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