XbFraFrag
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB54799 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| CAMPPW01.dat.gz | Other | |||
| CAMPPW01.fasta.gz | Fasta.gz | |||
| CAMPPW01.master.dat | Other | |||
| CAMPPX01.dat.gz | Other |
Items per page: 5 1 - 5 of 13 |
Similar Datasets
Project description:Fragum fragum (heart cockle), genomic and transcriptomic data
| PRJEB54798 | ENA
Project description:Development and function of the human heart depend on the dynamic control of tissue-specific gene expression by distant-acting transcriptional enhancers. While large numbers of heart enhancers have been identified using the mouse as a model system, many of these regulatory sequences are poorly conserved in the human genome. To generate an accurate genome-wide map of human heart enhancers, we used an epigenomic enhancer discovery approach and identified ~6,200 candidate enhancer sequences directly from fetal and adult human heart tissue. Consistent with their predicted function, these elements were markedly enriched near genes implicated in heart development, function and disease. To further validate their in vivo enhancer activity, we tested 65 of these human sequences in a transgenic mouse enhancer assay and observed that 43 (66%) drove reproducible reporter gene expression in the heart. These results support the discovery of a genome-wide set of non-coding sequences highly enriched in human heart enhancers which is likely to facilitate down-stream studies of the role of enhancers in development and pathological conditions of the heart. Examination of AcCBP/p300 binding in human adult heart, human fetal (16wk) heart and mouse postnatal day 2 heart
2011-12-04 | E-GEOD-32587 | biostudies-arrayexpress
Project description:Tbx20 is a transcription factor important for heart development. To assess the role of Tbx20 in the adult heart, we sought to identify regulatory regions, gene targets and pathways regulated by this TF. To this end, we used chromatin immunoprecipitation (ChIP) of Tbx20 fused to GFP to locate binding sites in the genome of 8 weeks whole heart mouse tissue. Analysis of 1 Tbx20-GFP ChIP sample of adult mouse whole heart against whole heart input
2011-11-21 | E-GEOD-29636 | biostudies-arrayexpress
Project description:Accurate control of tissue-specific gene expression plays a pivotal role in heart development. However, few cardiac transcriptional enhancers have thus far been identified. Extreme non-coding sequence conservation successfully predicts enhancers active in many tissues, but fails to identify substantial numbers of enhancers active in the heart. We used ChIP-seq with the enhancer-associated protein p300 from mouse embryonic heart tissue to identify over three thousand candidate heart enhancers genome-wide. In contrast to other studied tissues at this time-point, most candidate heart enhancers are not deeply conserved in vertebrate evolution. Nevertheless, the testing of 130 candidate regions in a transgenic mouse assay revealed that most of them reproducibly function as enhancers active in the heart, irrespective of their degree of evolutionary constraint. These results provide evidence for tissue-dependent differences in evolutionary constraint of enhancers acting through the transcriptional co-activator p300 at this time-point, and identify a large population of poorly conserved heart enhancers. Examination of p300 binding in embryonic stage 11.5 mouse heart and midbrain
2010-08-22 | E-GEOD-22549 | biostudies-arrayexpress
Project description:Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in heart failure. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during the evolution of heart failure. BET inhibition suppresses cardiomyocyte hypertrophy in a cell-autonomous manner, confirmed by RNA interference in vitro. Following both pressure overload and neurohormonal stimulation, BET inhibition potently attenuates pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to heart failure pathogenesis. Specifically, BET bromodomain inhibition in mice abrogates pathology-associated pause release and transcriptional elongation, thereby preventing activation of cardiac transcriptional pathways relevant to the gene expression profile of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in heart failure. ChIP-Seq of mouse heart tissues from mice induced with heart failure and treated with JQ1 BET bromodomain inhibitor
2013-08-06 | E-GEOD-46668 | biostudies-arrayexpress
Project description:Background: To better understand the role DNA methylation plays in regulating gene expression in the developng heart and furthermore the role it plays in heart development we performed genome wide DNA methylation profiling of embryonic hearts at embryonic day (E)11.5 and E14.5 using methyl sensitive tiny fragment enrichment coupled with massive parallel sequencing by using the methyl-sensitive restriction enzyme HpyCH4IV, recognition site 'ACGT'. Results: We found that global methylation remains stable at analyzed 'ACGT' sites (1.64 million site) in developing hearts between E11.5 and E14.5. However, differential methylation was identified at individual loci enriched at genes involved in heart development suggesting a role for DNA methylation in the developing heart. Used Methyl Sensitive Tiny Fragment Enrichment/Massive Parallel Sequencing (MSFE/MPS) to assay methylation at 'ACGT' sites throughout the genome and generate a developmental profile of DNA methylation in the embryonic heart and to identify differences between developing mouse hearts at E11.5 and E14.5.
2014-06-27 | E-GEOD-55141 | biostudies-arrayexpress
Project description:The contraction pattern of the heart relies on the activation and conduction of the electrical impulse. Perturbations of cardiac conduction have been associated with congenital and acquired arrhythmias as well as cardiac arrest. The pattern of conduction depends on the regulation of heterogeneous gene expression by key transcription factors and transcriptional enhancers. Here, we assessed the genome-wide occupation of conduction system–regulating transcription factors TBX3 in the mouse heart, uncovering cardiac enhancers throughout the genome. Examination of the cardiac transcription factor Tbx3 in adult mouse heart
2013-03-05 | E-GEOD-44821 | biostudies-arrayexpress
Project description:Through integration of GATA4 genome-wide occupancy and RNA-seq dataset in embryonic conditional knockout heart, we identified a class of the master cardiac regulator GATA4 bound enhancers. With combinatorial assembly of chromatin signatures, we further refined that a unique type of fetal distal GATA4 enhancers enriched for H3K27ac, H3K4me1, but not for H3K4me3 and RNA polymerase II, are reinstated in adult hypertrophic heart. Study Gata4 and histone modifications in E12.5, Adult, Banding and Sham, and to correlate to gene expression and heart function
2014-08-13 | E-GEOD-52123 | biostudies-arrayexpress