Identification of H3K27ac-marked enhancers in bovine satellite cells during differentiation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA745179 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15087366.fastq.gz | Fastqsanger.gz | |||
| SRR15087367.fastq.gz | Fastqsanger.gz | |||
| SRR15087368.fastq.gz | Fastqsanger.gz | |||
| SRR15087369.fastq.gz | Fastqsanger.gz | |||
| SRR15087370.fastq.gz | Fastqsanger.gz |
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Project description:In this study we isolated satellite cells from skeletal muscle from two Angus-crossbred steers, initially cultured them in growth medium for proliferation, and then in differentiation medium to induce them to differentiate and fuse into myotubes. We used ChIP-seq to identify enhancers marked with H3K27ac, i.e., active enhancers, from these cells immediately before and two days after induction of differentiation. Nearly 20,000 and 50,000 H3K27ac-marked enhancers were consistently identified from two biological replicates of before- and during-differentiation bovine satellite cells, respectively.
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Project description:Satellite cells are myogenic precursor cells in adult skeletal muscle and play a crucial role in skeletal muscle repair, remodeling, and maintenance. Like myoblasts, satellite cells have the ability to proliferate, differentiate, and fuse to form multinucleated myofibers. In this study we aimed to identify the enhancers and the transcription factors binding to these enhancers that control gene expression in proliferating and differentiating bovine satellite cells. Using ChIP-seq, we identified 56,973 and 54,470 active enhancers, genomic regions marked with both H3K4me1 and H3K27ac, and 50,956 and 59,174 repressed enhancers, genomic regions marked with H3K27me3, in proliferating and differentiating bovine satellite cells, respectively. Motif enrichment analyses revealed many transcription factors including the AP-1 family transcription factors that regulate gene expression in proliferating bovine satellite cells and many transcription factors besides MyoG that regulate gene expression in differentiating bovine satellite cells.
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Project description:In this study we analyzed the bovine satellite cells with single-cell RNA sequencing (scRNA-seq). We isolated muscle satellite cells from a male calf, cultured them in growth medium for a week, and then constructed two scRNA-seq libraries from them using the 10x Genomics platform. Next generation sequencing yielded 860 million reads. Cell calling analyses revealed that these reads represented 15 cell clusters that differed in gene expression profile from a total of 19,096 individual cells.
2022-01-17 | GSE184128 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE23907: Histone H3K27ac separates active from poised enhancers and predicts developmental state (gene expression data) GSE24164: ChIP-Seq of chromatin marks at distal enhancers in Mouse Embryonic Stem Cells and adult tissues. Refer to individual Series
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Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer âbrakeâ to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. mRNA-seq of parental and RACK7-KO ZR-75-30 cells
2016-04-07 | E-GEOD-71325 | biostudies-arrayexpress
Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer âbrakeâ to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. nascent RNA-seq of parental and RACK7-KO cells
2016-04-07 | E-GEOD-71326 | biostudies-arrayexpress
Project description:Histone modifications are now well-established regulators of transcriptional programs that distinguish distinct cell states. However, the kinetics of histone modification and their role in mediating rapid, signal-responsive changes in gene expression have been little studied on a genome-wide scale. Vascular endothelial growth factor A (VEGF), a major regulator of angiogenesis, rapidly triggers changes in transcriptional activity of human umbilical vein endothelial cells (HUVECs). Here we used chromatin immunoprecipitation and high throughput sequencing (ChIP-seq) to measure genome-wide changes in histone H3 acetylation at lysine 27 (H3K27ac), a marker of active enhancers {Kharchenko et al., 2011, Nature, 471, 480-5;Zentner et al., 2011, Genome Res, 21, 1273-83;Rada-Iglesias et al., 2011, Nature, 470, 279-83; Creyghton et al., 2010, Proc Natl Acad Sci U S A, 107, 21931-6 }, after 0, 1, 4, and 12 hours of VEGF stimulation. We show that sites with greatest H3K27ac changes were associated tightly with p300, a histone acetyltransferase. This dynamic H3K27ac signature defined transcriptional elements that are functionally linked to angiogenesis, participate in rapid VEGF-stimulated changes in chromatin conformation, and mediate VEGF-induced transcriptional responses. Dynamic H3K27ac deposition required p300 activity and did not involve altered nucleosome occupancy. Our results demonstrate that capture of dynamic changes in H3K27ac provides a new approach to define the activity of functional genomic elements and implicate epigenetic modifications in rapid signal-responsive transcriptional regulation. ChiP-seq timecourse of H3K27ac, ETS1, p300 chromatin occupancy, mRNA expression and DNA hypersensitivity of HUVEC cells stimulated with VEGF for 0, 1, 4, and 12 hours
2013-03-31 | E-GEOD-41166 | biostudies-arrayexpress
Project description:Primed enhancers are marked by histone H3K4 mono-methylation (H3K4me1), and the conversion to active enhancers involves acetylation of histone H3K27 (H3K27Ac). However, whether active enhancers are regulated remains unclear. Here we report a biochemical complex consisting of a potential chromatin reader (RACK7) and a histone demethylase (KDM5C) that occupies many active enhancers in a breast cancer cell line. Loss of RACK7 or KDM5C results in hyperactive enhancers marked by H3K4me3 and H3K27Ac, and characterized by an increased eRNA transcription and elevated expression of nearby genes. Loss of RACK7 or KDM5C also leads to increased cell invasion and migration, and enhanced tumor growth. We propose that RACK7/KDM5C functions as an enhancer âbrakeâ to ensure appropriate enhancer activities in the cell. Our findings provide important insight into histone H3K4 methylation dynamics at enhancers and reveal a molecular mechanism that controls the activities of active enhancers, which when compromised, can contribute to tumorigenesis. ChIP-seq data of RACK7, KDM5C and histone modifications in parental and RACK7-KO ZR-75-30 cells.
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