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HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [ChIP-seq]

ABSTRACT: HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [ChIP-seq]

PROVIDER: PRJNA756788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15561000_1.fastq.gz	Fastqsanger.gz
	SRR15561000_2.fastq.gz	Fastqsanger.gz
	SRR15561001_1.fastq.gz	Fastqsanger.gz
	SRR15561001_2.fastq.gz	Fastqsanger.gz
	SRR15561002_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [ChIP-seq]

Project description:Zygotic genome activation (ZGA) is an impressed biological event following fertilization during early embryo development. Precise reprogramming of epigenetic modifications (e.g. histone H3 lysine 27 acetylation, H3K27ac) have been found contribute to safeguard ZGA in zebrafish and Drosophila, but the dynamic of H3K27ac and the underlying regulation mechanism in mammal embryos are still enigmatic yet. As the main erasers for histone acetylation, histone deacetylase 1 and 2 (HDAC1 and HDAC2) are reported essential for mouse oogenesis and embryo lineage development, while it is unclear if they are functional for ZGA. Here, we observed significant global decrease of H3K27ac during ZGA in both mouse and bovine embryos, and accumulation of HDAC1/2 is responsible for the decline of H3K27ac. Repression of HDAC1/2 by dominant negative mutation led to arrested development at late 2-cell stage in mouse embryos, accompanied by downregulation of genes supposed to be expressed during ZGA. ChIP-seq revealed abnormal distribution of H3K27ac, and DUX participates in H3K27ac aberrant hyper-acetylation in embryos overexpressed mutant HDAC1/2. Moreover, suppression of HDAC1/2 also restrains H3K4me3 removal at gene body regions via impeding expression of KDM5s during mouse ZGA, and compensatory exogenous Kdm5b mRNA can fix the exceeding H3K4me3 and failed ZGA. Intriguingly, function of HDAC1/2 seems to be conservative between mouse and bovine embryos. Together, this study reveals that HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3.

2022-05-21 | GSE182554 | GEO

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [RNA-seq]

2022-05-21 | GSE182553 | GEO

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3

Project description:HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3

| PRJNA756787 | ENA

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [RNA-seq]

Project description:HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3 [RNA-seq]

| PRJNA756789 | ENA

HDAC1/2 is indispensable for mouse and bovine ZGA via regulating distribution of H3K27ac and H3K4me3

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-05-21 | GSE182555 | GEO

Metabolic control of histone acetylation for precise and timely regulation of minor ZGA in early mammalian embryos

Project description:We report that oxidized nicotinamide adenine dinucleotide (NAD+) is indispensable for mouse pre-implantation development. NAD+ could avoids excessive minor zygotic gene activation (ZGA) by cooperating with SIRT1 to remove zygotic H3K27ac. In human, NAD+ supplement can promote the removal of zygotic H3K27ac and benefit pre-implantation development. Our findings demonstrate that precise and timely regulation of minor ZGA is controlled by metabolic dynamics, and enhance our understanding of the metabolism of mammalian early embryos.

2022-10-05 | GSE185653 | GEO

NSD1-mediated HDAC1 recruitment reduces H3K27ac at active enhancers to safeguard associated gene expression

Project description:Epigenetics, especially histone marks, functions beyond the DNA sequences to regulate gene expression. Depletion of NSD1, which catalyzes H3K36me2, led to both up- and down-regulation of gene expression, indicating NSD1 is associated with both active and repressed gene expression. It’s known that NSD1 regulates the deposition and expansion of H3K27me3, a repressive mark for gene expression, to keep active gene transcription. However, how NSD1 functions to repress gene expression is largely unknown. Here, we found that, when NSD1 was knocked out in mouse embryonic stem cells (mESCs), H3K27ac increased correlatively with the decrease of H3K36me2 at active enhancers, which is associated with mesoderm differentiation genes, leading to elevated gene expression. Mechanistically, NSD1 recruits HDAC1, the deacetylase of H3K27ac, to chromatin. Moreover, HDAC1 knockout (KO) recapitulates the increase of H3K27ac at active enhancers as the NSD1 depletion. Together, we propose that NSD1 deposits H3K36me2 and recruits HDAC1 at active enhancers to serve as a ‘safeguard’, preventing further activation of active enhancer-associated genes.

2021-06-15 | GSE169049 | GEO

Dynamic landscapes of H3K27ac in mouse preimplantation embryos

Project description:Histone acetylation H3K27ac is a well-established chromatin marker for active enhancers and promoters. However, reprogramming dynamics of H3K27ac during maternal-to-zygotic transition (MZT) in mammalian embryos has not been well studied. By profiling the allelic landscape of H3K27ac during mouse MZT, here we show that H3K27ac undergoes three waves of rapid global transitions from oocyte to 2-cell stages. Notably, germinal vesicle (GV) oocyte and zygote are globally hyperacetylated by forming noncanonical broad H3K27ac domains that correlate with broad H3K4me3 and open chromatin. H3K27ac also marks genomic regions primed for activation including ZGA gene promoters, retrotransposons, and active alleles of imprinted genes. Importantly, both CBP/p300 and HDAC activities play important roles in regulating the H3K27ac dynamics and are essential for pre-implantation development. Specifically, CBP/p300 deposits broad H3K27ac domains in zygotes and open condensed chromatin at putative enhancers to ensure proper ZGA. In contrast, HDACs mediate the broad to canonical H3K27ac transition to safeguard ZGA by preventing premature expression of developmental genes and promoting ZGA gene activation. Our study demonstrates that coordinated activities of CBP/p300 and HDACs during mouse MZT are essential for ZGA and mouse pre-implantation development.

2022-08-30 | GSE207222 | GEO

Genomewide profiling of H3K27ac following HDAC1/2 inhibition with romidepsin and evaluation of co-regulated mechanisms by HDAC2 and SMAD3 in BTSC genome.

Project description:To investigate the impact on global H3K27ac patterns following HDAC1/2 inhibition with romidepsin, we performed using ChIP-seq using formaldehyde crosslinked BT67 romidepsin treated versus vehicle treated cells.

2023-07-09 | GSE214926 | GEO

Computational inference of H3K4me3 and H3K27ac domain length.

Project description:Background. Recent epigenomic studies have shown that the length of a DNA region covered by an epigenetic mark is not just a byproduct of the assaying technologies and has functional implications for that locus. For example, expanded regions of DNA sequences that are marked by enhancer-specific histone modifications, such as acetylation of histone H3 lysine 27 (H3K27ac) domains coincide with cell-specific enhancers, known as super or stretch enhancers. Similarly, promoters of genes critical for cell-specific functions are marked by expanded H3K4me3 domains in the cognate cell type, and these can span DNA regions from 4-5kb up to 40-50kb in length. These expanded H3K4me3 domains are known as buffer domains or super promoters. Methods. To ask what correlates with-and potentially regulates-the length of loci marked with these two important histone marks, H3K4me3 and H3K27ac, we built Random Forest regression models. With these models, we computationally identified genomic and epigenomic patterns that are predictive for the length of these marks in seven ENCODE cell lines. Results. We found that certain epigenetic marks and transcription factors explain the variability of the length of H3K4me3 and H3K27ac marks across different cell types, which implies that the lengths of these two epigenetic marks are tightly regulated in a given cell type. Our source code for the regression models and data can be found at our GitHub page: https://github.com/zubekj/broad_peaks. Discussion. Our Random Forest based regression models enabled us to estimate the individual contribution of different epigenetic marks and protein binding patterns to the length of H3K4me3 and H3K27ac deposition patterns, therefore potentially revealing genomic signatures at cell specific regulatory elements.

| S-EPMC4793332 | biostudies-literature

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