High/low MNase-seq in foregut, Control and FOXA-TKD
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1040315 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26830860_1.fastq.gz | Fastqsanger.gz | |||
| SRR26830860_2.fastq.gz | Fastqsanger.gz | |||
| SRR26830861_1.fastq.gz | Fastqsanger.gz | |||
| SRR26830861_2.fastq.gz | Fastqsanger.gz | |||
| SRR26830862_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
Similar Datasets
Project description:Nucleosome occupancy and positioning were examined in foregut stage to compare control and FOXA-TKD using high/low MNase-seq
2024-01-10 | GSE247785 | GEO
Project description:In higher eukaryotes, enhancers and promoters share many properties, including binding of transcription factors, existing in open chromatin, and bidirectional transcription. Yet the structural features that distinguish enhancers and promoters are unclear. Genome-wide micrococcal nuclease (MNase) studies previously interpreted MNase hypersensitivity to indicate that active enhancers and promoters are nucleosome-free, yet other studies found histone variants and post-translational modifications at active enhancers. We find that prior MNase genomic studies have an overdigestion bias and that low-level MNase digestion, coupled with mapping core histones, reveals two classes of MNase-hypersensitive sites: at active promoters, which are nucleosome depleted, and at tissue-specific enhancers, which retain core histones and co-bound transcription factors substantially more than promoters. Hypersensitivity of active enhancer nucleosomes may reflect their preferential exposure in chromatin and can be maintained by pioneer transcription factors such as FoxA. These findings unveil fundamental differences in the chromatin structure of active enhancers and promoters.
2016-04-08 | GSE57558 | GEO
Project description:FoxA transcription factors are critical for liver development through their pioneering activity, which initiates a highly complex network thought to become resistant to the loss of any individual hepatic transcription factor via mutual redundancy. To investigate the dispensability of FoxA factors for this regulatory network, we ablated all FoxA genes in the adult liver. Remarkably, loss of FoxA caused a rapid and massive reduction in the expression of key liver genes back to the low levels of the fetal prehepatic endoderm stage, leading to necrosis and lethality within days. Mechanistically, we found FoxA proteins to be required for maintaining chromatin activity, nucleosome positioning and binding by other hepatic transcription factors. Thus, the hepatic gene regulatory network is dependent on the FoxA proteins throughout life.
2020-07-10 | GSE140423 | 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: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:Foregut organogenesis is regulated by inductive interactions between the endoderm and the adjacent mesoderm. We identified genes induced in the foregut progenitors by the adjacent mesoderm. We used microarrays to detail the global programme of early foregut endoderm gene expression resulting from mesoderm induction and identified distinct classes of up-regulated genes during this process. Xenopus foregut endoderm explants cultured from Stages 15 to 23 either intact with mesoderm or as endoderm alone. Total RNA was isolated from the endoderm of these two culture conditions in quadruplicate and were subjected to Affymetrix microarray analysis.
2012-06-11 | E-GEOD-38654 | biostudies-arrayexpress
Project description:Proof-of-concept for Mnase-SSP: a variant of Mnase-seq. Mnase-SSP dramatically increases the representation of short fragments of nucleolytically-digested DNA, enabling simultaneous analysis of transcription factor binding and nucleosome occupancy using the same assay. We used MNase-SSP to demarcate chromatin architecture at murine promoters and at transcription factor binding sites in murine embryonic stem cells. Are results reveal heterogeneity in the binding mode of C2H2 zinc fingers like Ctcf and Rest, demonstrating that Mnase-SSP, and SSP in general, as a flexible platform for profiling nucleolytically digested DNA for MNase-seq, MNase-ChIP, or CUT&RUN with reduced bias.
2019-02-12 | GSE125053 | GEO
Project description:Foregut organogenesis is regulated by inductive interactions between the endoderm and the adjacent mesoderm. We identified genes induced in the foregut progenitors by the adjacent mesoderm. We used microarrays to detail the global programme of early foregut endoderm gene expression resulting from mesoderm induction and identified distinct classes of up-regulated genes during this process.
2012-06-12 | GSE38654 | GEO
Project description:Adult Drosophila foregut contains a diverse set of tissue and cell types. We applied single cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) to delineate the cellular composition and molecular profile of the foregut and its associated physiological functions.
2024-03-05 | GSE243037 | GEO
Project description:In the HBV transgenic mouse model of chronic infection, the forkhead box protein A/hepatocyte nuclear factor 3 (Foxa/HNF3) family of pioneer transcription factors are required to support postnatal viral demethylation and subsequent HBV transcription and replication. Liver-specific Foxa-deficient mice with hepatic expression of only Foxa3 do not support HBV replication but display biliary epithelial hyperplasia with bridging fibrosis. However, liver-specific Foxa-deficient mice with hepatic expression of only Foxa1 or Foxa2 also successfully restrict viral transcription and replication but display only minimal alterations in liver physiology. These observations suggest that the level of Foxa activity, rather than the combination of specific Foxa genes, is a key determinant of HBV biosynthesis. Together, these findings suggest that targeting Foxa activity could lead to HBV DNA methylation and transcriptional inactivation, resulting in the resolution of chronic HBV infections which are responsible for approximately one million deaths annually worldwide.
2024-07-16 | GSE263120 | GEO