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TTC7A deficiency Impacts the H3K27ac and H3K27me3 histone marks

ABSTRACT: TTC7A deficiency Impacts the H3K27ac and H3K27me3 histone marks

PROVIDER: PRJEB22728 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR2133990.fastq.gz	Fastqsanger.gz
	ERR2134000.fastq.gz	Fastqsanger.gz
	ERR2133991.fastq.gz	Fastqsanger.gz
	ERR2134001.fastq.gz	Fastqsanger.gz
	ERR2133992.fastq.gz	Fastqsanger.gz

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TTC7A deficiency Impacts the H3K27ac and H3K27me3 histone marks

Project description:Transcriptional regulation relies upon multiple nuclear processes among which histone modifications constitute a key component. To further decipher the nuclear changes resulting from TTC7A deficiency, we performed ChIP-Seq of H3K27ac and H3K27me3 histone marks associated with transcriptional activation and repression respectively.

2018-10-19 | E-MTAB-5940 | biostudies-arrayexpress

CUT&RUN against H3K27ac and H3K27me3 on WT and TKO ESCs (D0), and D2, D4 EpiLCs

Project description:We investigate the impact of DNA methylation on chromatin epigenetic marks during epiblast differentiation. To this end, we used in vitro Epiblast-like cell (EpiLC) differentiation on WT and DNA-methylation free TKO murine ESCs. We next performed CUT&RUN against H3K27me3 and H3K27ac at D0, D2 and D4.

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Distribution of H3K27me3, H3K27ac, and H3K4me1 in E(z) temperature sensitive cells

Project description:PcG protein complex PRC2 is a methyltransferase specific for histone H3 lysine27, and H3K27me3 is essential for stable transcription silencing. Here we have determined genomic distributions of H3K27me3, H3K27ac, and H3K4me1 in cultured Drosophila E(z) temperature sensitive cells at 25°C and 31°C where E(z) is largely inactivated by hybridization of ChIP products with tiling microarrays. Genomic distributions of H3K27me3, H3K27ac, and H3K4me1 in cultured Drosophila E(z) temperature sensitive cells (EZ2-2) at 25°C and 31°C where E(z) is largely inactivated by hybridization of ChIP products with tiling microarrays

2015-05-14 | E-GEOD-61262 | biostudies-arrayexpress

Role of H3K4me1 and H3K27ac histone marks in aging Drosophila

Project description:Temporal and spatial gene expression patterns are regulated by enhancer-specific histone modifications H3K4me1 and H3K27ac. To better understand age-dependent alteration of these enhancer marks, we analysed their genome-wide profiles and compared against changes in gene expression in the head tissues harvested from young Day 10 and D50 male Drosophila. The genome-wide binding patterns of H3K4me1 and H3K27ac remain highly similar (>85%) during ageing with marginally higher signals for both marks in older Day 50 flies. Signals were significantly higher in Day 50 flies near the transcription start sites for H3K4me1 whereas for H3K27ac, signals were significantly higher in Day 50 flies globally. Interestingly, analysis using MACS bdgdiff identified “x” H3K4me1 and “y” H3K27ac differential peaks that correlated with distinct sets of age-dependent differential expressed genes (DEG). Most of the H3K4me1 differential peaks (percentage of x) are located within the gene body of DEGs that are associated with RNA and metabolic processes. On the other hand, majority of differential H3K27ac peaks (percentage of y) are located 5 kb upstream of TSS of DEG enriched for various immune responses. Our results suggest that while both enhancer marks do not undergo significant global reconfiguration during aging, they are likely to be involved in activating independent sets of genes through distinct transcription activators.

2023-12-31 | GSE210427 | GEO

Enrichment of various epigenetic histone marks in human myoblasts

Project description:WS234 cells are an immortalized human cell line. Here we have explored the distribution of histone marks (H3K27me3, H3K27ac, H3K4me3, H3K4me1, and H3K9me3) across the genome in proliferative conditions.

2024-06-25 | GSE267354 | GEO

Identify acetylation marks in adult mouse L4 vertebrae gene promoter regions from maternal high fat diet dams using H3K27ac ChIP-Seq

Project description:Genes with increased H3K27ac marks in their promoters were found in adult mice L4 vertebrae from mice using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated due to maternal or offspring high fat diet would allow for better treatments to combat bone loss to be developed.

2022-05-31 | E-MTAB-11718 | biostudies-arrayexpress

Role of H3K4me1 and H3K27ac histone marks in aging Drosophila

Project description:Role of H3K4me1 and H3K27ac histone marks in aging Drosophila

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Identify acetylation marks from embryonic calvaria cell gene promoter regions from maternal high fat or control diet dams using H3K27ac ChIP-Seq.

Project description:Genes with increased H3K27ac marks in their promoters were found in mice embryonic calvaria cells using H3K27ac ChIP-Seq. Recent data suggests that in animals and humans that a maternal diet high in fat leads to poor bone growth and development in offspring. Genes with increased H3K27ac epigenetic marks normally have higher levels of expression. Understanding which genes are being upregulated in the offspring due to maternal diet would allow for better treatments to combat bone loss to be developed.

2022-05-31 | E-MTAB-11712 | biostudies-arrayexpress

Maternal high-fat diet modifies epigenetic marks H3K27me3 and H3K27ac in bone to regulate offspring osteoblastogenesis in mice.

Project description:Studies from both humans and animal models indicated that maternal chronic poor-quality diet, especially a high fat diet (HFD), is significantly associated with reduced bone density and childhood fractures in offspring. When previously studied in a rat model, our data suggested that maternal HFD changes epigenetic marks such as DNA methylation and histone modifications to control osteoblast metabolism. In mouse embryonic and postnatal offspring bone samples, a ChIP-sequencing (ChIP-Seq)-based genome-wide method was used to locate the repressive histone mark H3K27me3 (mediated via the polycomb histone methyltransferase, Ezh2) and expressive histone mark H3K27ac (p300/CBP mediated) throughout the genome. Using isolated mouse embryonic cells from foetal calvaria (osteoblast-like cells), H3K27me3 ChIP-Seq showed that 147 gene bodies and 26 gene promoters in HFD embryotic samples had a greater than twofold increase in H3K27me peaks compared to controls. Among the HFD samples, Pthlh and Col2a1 that are important genes playing roles during chondro- and osteogenesis had significantly enriched levels of H3K27me3. Their decreased mRNA expression was confirmed by real-time PCR and standard ChIP analysis, indicating a strong association with Ezh2 mediated H3K27me3 epigenetic changes. Using embryonic calvaria osteoblastic cells and offspring bone samples, H3K27ac ChIP-Seq analysis showed that osteoblast inhibitor genes Tnfaip3 and Twist1 had significantly enriched peaks of H3K27ac in HFD samples compared to controls. Their increased gene expression and association with H3K27ac were also confirmed by real-time PCR and standard ChIP analysis. These findings indicate that chronic maternal HFD changes histone trimethylation and acetylation epigenetic marks to regulate expression of genes controlling osteoblastogenesis.

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CUT&RUN chromatin profiling of H3K4me3, H3K27ac and H3K9me3 histone marks in spermatids and spermatocytes

Project description:Spermatogenesis is a recurring differentiation process that results in the production of male gametes within the testes. During this process, spermatogonial stem cells differentiate to form spermatocytes, which undergo two rounds of meiotic division to form haploid spermatids. Throughout spermiogenesis, round spermatids elongate to form mature sperm. To profile changes in chromatin marks between spermatocytes and spermatids, we generated CUT&RUN data of H3K4me3, H3K27ac and H3K9me3 marks in sorted spermatocytes and spermatids.

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