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Pioneer transcription factor FoxA maintains an accessible nucleosome configuration at enhancers for tissue-specific gene activation [ChIP-seq]

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE77670 | GEO | 2016/04/08

SECONDARY ACCESSION(S): PRJNA311179

REPOSITORIES: GEO

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Pioneer transcription factor FoxA maintains an open nucleosome configuration for tissue-specific gene activation [MNase-Seq]

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

Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [MNase-Seq]

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

Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-Seq]

2016-04-08 | GSE57557 | GEO

Hypersensitive Nucleosomes in Chromatin Are Intrinsic to the Structure of Active, Tissue-Specific Enhancers [ChIP-exo]

2016-04-08 | GSE57556 | GEO

Nucleosome binding by the pioneer transcription factor OCT4

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

CLK:BMAL1 is a pioneer-like transcription factor [CLK_ChIP]

Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. Mouse liver CLK ChIP-Seq signal on Mnase-digested or sonicated chromatin, at 2 different time point (ZT22 and ZT06) from the same mice. Libraries were sequenced using Ilumina HiSeq2000. For Mnase-digested chromatin, libraries contained a mononucleosome insert (e.g., ~147bp), whereas the insert was ~150-300bp for sonicated chromatin.

2014-01-06 | E-GEOD-47144 | biostudies-arrayexpress

Genome-wide profiling of nucleosome sensitivity and chromatin accessibility in D. melanogaster [MNase]

Project description:Nucleosome structure and positioning play pivotal roles in gene regulation, DNA repair and other essential processes in eukaryotic cells. Nucleosomal DNA is thought to be uniformly inaccessible to DNA binding and processing factors, such as MNase. Here, we show, however, that nucleosome accessibility and sensitivity to MNase varies. Digestion of Drosophila chromatin with two distinct concentrations of MNase revealed two types of nucleosomes: sensitive and resistant. MNase-resistant nucleosome arrays are less accessible to low concentrations of MNase, whereas MNase-sensitive arrays are degraded by high concentrations. MNase-resistant nucleosomes assemble on sequences depleted of A/T and enriched in G/C containing dinucleotides. In contrast, MNase-sensitive nucleosomes form on A/T rich sequences represented by transcription start and termination sites, enhancers and DNase hypersensitive sites. Lowering of cell growth temperature to ~10°C stabilizes MNase-sensitive nucleosomes suggesting that variations in sensitivity to MNase are related to either thermal fluctuations in chromatin fiber or the activity of enzymatic machinery. In the vicinity of active genes and DNase hypersensitive sites nucleosomes are organized into synchronous, periodic arrays. These patterns are likely to be caused by “phasing” nucleosomes off a potential barrier formed by DNA-bound factors and we provide an extensive biophysical framework to explain this effect. Mnase-seq, Mnase-ChIP-seq of Drosophila melanogaster embryo and S2 cells chromatin

2015-09-17 | E-GEOD-69177 | biostudies-arrayexpress

Genome-wide profiling of nucleosome sensitivity and chromatin accessibility to MNase in D. melanogaster [RNA-seq]

2015-09-17 | E-GEOD-69335 | biostudies-arrayexpress

CLK:BMAL1 is a pioneer-like transcription factor [MNase-Seq]

Project description:The mammalian circadian clock relies on the master genes CLOCK (CLK) and BMAL1 and drives rhythmic gene expression to regulate biological functions under circadian control. We recently uncovered a surprising disconnect between the rhythmic binding of CLK:BMAL1 on DNA and the transcription of its target genes, suggesting that they are regulated by as yet uncharacterized mechanisms. Here we show that rhythmic CLK:BMAL1 DNA binding promotes rhythmic chromatin opening. The underlying mechanisms include CLK:BMAL1 binding to nucleosomes and rhythmic chromatin modifications, including the incorporation of the histone variant H2A.Z. This rhythmic chromatin remodeling mediates the rhythmic binding of other transcription factors adjacent to CLK:BMAL1, suggesting that the activity and the tissue-specific expression of these other transcription factors contribute to the genome-wide CLK:BMAL1 heterogeneous transcriptional output. These data therefore indicate that the clock regulation of transcription relies on the rhythmic regulation of chromatin accessibility and suggest that the concept of pioneer function extends to acute gene regulation, well beyond the current confines of developmental/cell specification. Mouse liver nucleosome profile assayed by MNase-Seq over 6 time points of the 24h light:dark cycle (4 wild-type and 4 Bmal1-/- mice per time point). Illumina libraries containing a mononucleosome insert were sequenced using Ilumina HiSeq2000.

2014-01-06 | E-GEOD-47142 | biostudies-arrayexpress

Effect of NKX2-5 or ETS1 on GATA4 pioneer activity [fibroblast]

Project description:GATA4 is a pioneer transcription factor. The mechanisms by which pioneer factors select and occupy specific loci, open chromatin, and activate enhancers is not well understood. To address the influence of partner, non-pioneer factors on pioneer factor activity, we analyzed the effect of NKX2-5 or ETS1 on GATA4 pioneer activity. NIH3T3 cells were transduced with lentivirus to obtain stable cell lines that express GFP (control), GATA4 (G), NKX2-5 (N), ETS1 (E), GATA4+NKX2-5 (GN), and GATA4+ETS1 (GE). We measured chromatin accessibility using ATAC-seq, and enhancer activation using H3K27ac. From these measurements we determined GATA4, GATA4+ETS, and GATA4+NKX2-5 pioneer binding, pioneer opening, and pioneer enhancer activation. Our results show that ETS1 or NKX2-5 alter GATA4 pioneer binding, opening, and enhancer activation.

2021-07-01 | GSE155652 | GEO

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