Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA144639 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR309237.fastq.gz | Fastqsanger.gz | |||
| SRR309238.fastq.gz | Fastqsanger.gz | |||
| SRR309239.fastq.gz | Fastqsanger.gz | |||
| SRR309240_1.fastq.gz | Fastqsanger.gz | |||
| SRR309240_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 34 |
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Project description:The regulatory elements that direct tissue-specific gene expression in the developing mammalian embryo remain largely unknown. Although chromatin profiling has proven to be a powerful method for mapping regulatory sequences in cultured cells, chromatin states characteristic of active developmental enhancers have not been directly identified in embryonic tissues. Here we use whole transcriptome analysis coupled with genome-wide profiling of H3K27ac and H3K27me3 to map chromatin states and enhancers in mouse embryonic forelimb and hindlimb. We show that gene expression differences between forelimb and hindlimb, and between limb and other embryonic cell types, are correlated with tissue-specific H3K27ac signatures at promoters and distal sites. Using H3K27ac profiles, we identified 28,377 putative enhancers, many of which are likely to be limb-specific based on strong enrichment near genes highly expressed in the limb and comparisons with tissue-specific p300 sites and known enhancers. We describe a chromatin state signature associated with active developmental enhancers, defined by high levels of H3K27ac marking, nucleosome displacement, hypersensitivity to sonication, and strong depletion of H3K27me3. We also find that developmental enhancers exhibit components of this signature, including hypersensitivity, H3K27ac enrichment and H3K27me3 depletion, at lower levels in tissues in which they are not active. Our results establish histone modification profiling as a tool for developmental enhancer discovery, and suggest that enhancers maintain an open chromatin state in multiple embryonic tissues independent of their activity level. Examination of genome wide H3K27ac and H3K27me3 histone modifications and gene expression in early mouse embryonic limb tissue.
2012-03-16 | E-GEOD-30641 | biostudies-arrayexpress
Project description:Tissue specific analysis of chromatin state reveals predictive signatures of enhancer activity during embryonic development
| PRJEB2454 | ENA
Project description:Cohesin is implicated in establishing tissue-specific DNA loops that target enhancers to promoters, and also localizes to sites bound by the insulator protein CTCF, which blocks enhancer-promoter communication. However, cohesin-associated interactions have not been characterized on a genome-wide scale. Here we performed chromatin interaction analysis with paired-end tag sequencing (ChIA-PET) of the cohesin subunit SMC1A in developing mouse limb. We identified 2,264 SMC1A interactions, of which 1,491 (65%) involved sites co-occupied by CTCF. SMC1A participates in tissue- specific enhancer-promoter interactions and interactions that demarcate regions of correlated regulatory output. In contrast to previous studies, we also identified interactions between promoters and distal sites that are maintained in multiple tissues, but are poised in embryonic stem cells and resolve to tissue-specific activated or repressed chromatin states in the mouse embryo. Our results reveal the diversity of cohesin- associated interactions in the genome and highlight their role in establishing the regulatory architecture of development. Smc1a ChIA-PET, RNA-seq, chromatin state maps (H3K27ac, H3K27me3, H3K4m2), and CTCF and Smc1a binding in mouse embryonic limb bud (E11.5)
2013-05-22 | E-GEOD-42237 | biostudies-arrayexpress
Project description:The regulatory elements that direct tissue-specific gene expression in the developing mammalian embryo remain largely unknown. Although chromatin profiling has proven to be a powerful method for mapping regulatory sequences in cultured cells, chromatin states characteristic of active developmental enhancers have not been directly identified in embryonic tissues. Here we use whole transcriptome analysis coupled with genome-wide profiling of H3K27ac and H3K27me3 to map chromatin states and enhancers in mouse embryonic forelimb and hindlimb. We show that gene expression differences between forelimb and hindlimb, and between limb and other embryonic cell types, are correlated with tissue-specific H3K27ac signatures at promoters and distal sites. Using H3K27ac profiles, we identified 28,377 putative enhancers, many of which are likely to be limb-specific based on strong enrichment near genes highly expressed in the limb and comparisons with tissue-specific p300 sites and known enhancers. We describe a chromatin state signature associated with active developmental enhancers, defined by high levels of H3K27ac marking, nucleosome displacement, hypersensitivity to sonication, and strong depletion of H3K27me3. We also find that developmental enhancers exhibit components of this signature, including hypersensitivity, H3K27ac enrichment and H3K27me3 depletion, at lower levels in tissues in which they are not active. Our results establish histone modification profiling as a tool for developmental enhancer discovery, and suggest that enhancers maintain an open chromatin state in multiple embryonic tissues independent of their activity level.
2012-03-16 | GSE30641 | GEO
Project description:In this study, we explored the in vivo expression dynamics of tissue-specific non-coding RNAs in embryonic mouse tissues via in-depth transcriptome profiling. Overall, approximately 80% of validated in vivo enhancers show tissue-specific RNA expression that correlates with tissue-specific enhancer activity. Globally, we identified thousands of tissue-specifically transcribed non-coding regions (TSTRs) displaying various genomic hallmarks of bona fide enhancers. Together, our results demonstrate that tissue-specific eRNA expression is a common feature of in vivo enhancers, as well as a major source of extragenic transcription, and that eRNA expression signatures can be used to predict tissue-specific enhancers independent of known epigenomic enhancer marks. Examimation of total RNA expression in mouse heart and limb tissues collected at mouse embryonic day 11.5.
2014-09-11 | E-GEOD-58157 | biostudies-arrayexpress
Project description:Determining the spatial and temporal activity patterns of enhancers remains a challenge in the functional annotation of the human genome. Here, we performed genome-wide mapping of tissue-specific in vivo binding sites for the enhancer-associated protein p300 and assessed in transgenic mice the utility of this information in identifying enhancers and predicting their activity patterns. Chromatin immunoprecipitation followed by massively-parallel sequencing was used to identify p300-enriched sites in mouse embryonic day 11.5 (e11.5) forebrain, midbrain, and limb. In total, 4,686 genomic regions were enriched for p300 in vivo in at least one of these tissues. To determine whether p300-binding accurately identifies enhancers and predicts their activity patterns, we tested 86 of these regions in a transgenic mouse enhancer assay at e11.5. In 88% of the cases, p300-enriched sequences were reproducible enhancers, and in 91% of these cases p300 enrichment correctly predicted the tissues in which in vivo activity was observed. Our results indicate that in vivo mapping of p300 binding to non-coding DNA is a highly effective means for identifying enhancers and their associated spatial activity patterns. Examination of p300 binding in 3 embryonic stage 11.5 mouse tissues
2009-02-11 | E-GEOD-13845 | biostudies-arrayexpress
Project description:<p>We used epigenetic profiling to map active enhancers in the developing human limb and cortex as described in two published studies: <ul> <li>Cotney J, Leng J, Yin J, Reilly SK et al. The evolution of lineage-specific regulatory activities in the human embryonic limb. <a href="https://www.ncbi.nlm.nih.gov/pubmed/23827682">Cell 2013</a>;154(1):185-96. </li> <li>Reilly SK, Yin J, Ayoub AE, Emera D et al. Evolutionary changes in promoter and enhancer activity during human corticogenesis. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25745175">Science 2015</a>;347(6226):1155-9.</li> </ul> </p> <p> We also used ChIP-seq to map binding sites for the chromatin modifier <a href="https://www.ncbi.nlm.nih.gov/gene/?term=CHD8"><i>CHD8</i></a> in the developing human brain, as described in one published study: <ul> <li>Cotney J, Muhle RA, Sanders SJ, Liu L et al. The autism-associated chromatin modifier <a href="https://www.ncbi.nlm.nih.gov/gene/?term=CHD8"><i>CHD8</i></a> regulates other autism risk genes during human neurodevelopment. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25752243">Nat Commun 2015</a>;6:6404.</li> </ul> </p> <p> We are also depositing primary human sequence reads related to processed datasets in the Gene Expression Omnibus under the following accession numbers: <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE42413">GSE42413</a> (Cotney et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/23827682">2013</a>); <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE63649">GSE63649</a> (Reilly et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25745175">2015</a>); <a href="https://www.ncbi.nlm.nih.gov/gds/?term=GSE57369">GSE57369</a> (Cotney et al. <a href="https://www.ncbi.nlm.nih.gov/pubmed/25752243">2015</a>). </p>
| phs001226 | dbGaP
Project description:The evolution of human anatomical features likely involved changes in gene regulation during development. However, the nature and extent of human specific developmental regulatory functions remain unknown. We obtained a genome-wide view of cis regulatory evolution in human embryonic tissues by comparing the histone modification H3K27ac, which provides a quantitative readout of promoter and enhancer activity, during human, rhesus, and mouse limb development. Based on increased H3K27ac, we find that 13% of promoters and 11% of enhancers have gained activity on the human lineage since the human-rhesus divergence. These gains largely arose by modification of ancestral regulatory activities in the limb or potential co-option from other tissues and are likely to have heterogeneous genetic causes. Most enhancers that exhibit gain of activity in humans originated in mammals. Gains at promoters and enhancers in the human limb are associated with increased gene expression, suggesting they include molecular drivers of human morphological evolution. ChIP-Seq and RNA-Seq of autopod tissue of developing limb buds of Human (E33-E47), rhesus (E31-E36), and mouse (E10.5-E13.5). No raw data are provided for human samples. Human alignments were anonymized by removing sequence information and converting to bed format.
2013-07-02 | E-GEOD-42413 | biostudies-arrayexpress
Project description:Gene deserts spanning more than 500kb of non-protein coding genomic sequence are considered evolutionarily ancient and stable and are enriched in the vicinity of developmental regulator genes (Ovcharenko 2005). These extensive genomic regions typically harbor numerous conserved elements with predicted gene regulatory potential pointing to critical tissue-specific functions during development. Nevertheless, the biological necessity and underlying funtional enhancer landscapes of most gene deserts near developmental transcription factors (TFs) remain unknown, and it is unclear how precise pleiotropic expression patterns emerge from gene desert sequence. Here, we investigated the cis-regulatory architecture and function of a gene desert flanking the mouse Shox2 transcriptional regulator which itself is essential for embryonic limb, craniofacial, and cardiac pacemaker development. By combining epigenomic enhancer prediction, transgenic reporter validation and region-specific chromatin capture (C-HiC), we define the embryonic in vivo enhancer landscape and chromatin topology of the Shox2 gene desert. Targeted and context-specific genomic deletions uncover the gene desert not only as a regulator of embryonic survival through enhancer-mediated control of cardiac Shox2 expression, but also link distinct subsets of tissue-specific gene desert enhancers to the regulation of craniofacial patterning and proximal limb development. Our results hence identify the Shox2 gene desert as a fundamental genomic unit indispensable for pleiotropic patterning, robust organ morphogenesis and embryonic development progression by serving as a dynamic hub for tissue-specific developmental enhancers.
2024-06-01 | GSE232882 | GEO
Project description:Gene deserts spanning more than 500kb of non-protein coding genomic sequence are considered evolutionarily ancient and stable and are enriched in the vicinity of developmental regulator genes (Ovcharenko 2005). These extensive genomic regions typically harbor numerous conserved elements with predicted gene regulatory potential pointing to critical tissue-specific functions during development. Nevertheless, the biological necessity and underlying funtional enhancer landscapes of most gene deserts near developmental transcription factors (TFs) remain unknown, and it is unclear how precise pleiotropic expression patterns emerge from gene desert sequence. Here, we investigated the cis-regulatory architecture and function of a gene desert flanking the mouse Shox2 transcriptional regulator which itself is essential for embryonic limb, craniofacial, and cardiac pacemaker development. By combining epigenomic enhancer prediction, transgenic reporter validation and region-specific chromatin capture (C-HiC), we define the embryonic in vivo enhancer landscape and chromatin topology of the Shox2 gene desert. Targeted and context-specific genomic deletions uncover the gene desert not only as a regulator of embryonic survival through enhancer-mediated control of cardiac Shox2 expression, but also link distinct subsets of tissue-specific gene desert enhancers to the regulation of craniofacial patterning and proximal limb development. Our results hence identify the Shox2 gene desert as a fundamental genomic unit indispensable for pleiotropic patterning, robust organ morphogenesis and embryonic development progression by serving as a dynamic hub for tissue-specific developmental enhancers.
2024-06-01 | GSE232881 | GEO