Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268527 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1560370.fastq.gz | Fastqsanger.gz | |||
| SRR1560380.fastq.gz | Fastqsanger.gz | |||
| SRR1560390.fastq.gz | Fastqsanger.gz | |||
| SRR1560400.fastq.gz | Fastqsanger.gz | |||
| SRR1560371.fastq.gz | Fastqsanger.gz |
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Project description:Evolutionary changes in promoter and enhancer activity during human corticogenesis (human)
| PRJNA268529 | ENA
Project description:Evolutionary changes in promoter and enhancer activity during corticogenesis (non-human)
| PRJNA259649 | ENA
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:Evolutionary changes in gene regulation during cortical development likely contributed to the expansion and specialization of the cortex in humans. However, the lack of a regulatory map of the human embryonic cortex has hindered identification of these changes and the biological processes they influenced. We performed genome-wide epigenetic profiling to compare promoter and enhancer activity during corticogenesis in human, rhesus, and mouse. We identified 2,855 promoters and 8,996 enhancers that have gained activity in human based on increased epigenetic marking. To detect biological pathways enriched for these changes, we mapped promoters and enhancers exhibiting epigenetic gains onto modules of co-expressed genes constructed using spatio-temporally rich expression data from developing human cortex. We identified multiple modules enriched in human lineage epigenetic gains. Gains in enriched modules were associated with genes functioning in neuronal proliferation and migration, cortical patterning, and the extracellular matrix. Gain-enriched modules also showed correlated gene expression patterns and similar transcription factor binding site enrichments in promoters and enhancers, suggesting they are connected by common regulatory mechanisms. Our results reveal coordinated patterns of potential regulatory changes associated with conserved developmental processes in corticogenesis, providing insight into human cortical evolution.
2015-03-06 | GSE63648 | GEO
Project description:Evolutionary changes in gene regulation during cortical development likely contributed to the expansion and specialization of the cortex. However, the lack of a regulatory map of the embryonic cortex has hindered identification of these changes and the biological processes they influenced. We performed genome-wide epigenetic profiling to compare promoter and enhancer activity during corticogenesis in rhesus and mouse. We identified 2,855 promoters and 8,996 enhancers that have gained activity in based on increased epigenetic marking. To detect biological pathways enriched for these changes, we mapped promoters and enhancers exhibiting epigenetic gains onto modules of co-expressed genes constructed using spatio-temporally rich expression data from developing cortex. We identified multiple modules enriched in lineage epigenetic gains. Gains in enriched modules were associated with genes functioning in neuronal proliferation and migration, cortical patterning, and the extracellular matrix. Gain-enriched modules also showed correlated gene expression patterns and similar transcription factor binding site enrichments in promoters and enhancers, suggesting they are connected by common regulatory mechanisms. Our results reveal coordinated patterns of potential regulatory changes associated with conserved developmental processes in corticogenesis, providing insight into cortical evolution.
2015-03-06 | GSE60838 | GEO
Project description:This study aims to investigate the DNA methylation patterns at transcription factor binding regions and their evolutionary conservation with respect to binding activity divergence. We combined newly generated bisulfite-sequencing experiments in livers of five mammals (human, macaque, mouse, rat and dog) and matched publicly available ChIP-sequencing data for five transcription factors (CEBPA, HNF4a, CTCF, ONECUT1 and FOXA1). To study the chromatin contexts of TF binding subjected to distinct evolutionary pressures, we integrated publicly available active promoter, active enhancer and primed enhancer calls determined by profiling genome wide patterns of H3K27ac, H3K4me3 and H3K4me1.
2022-10-20 | E-MTAB-11946 | biostudies-arrayexpress
Project description:Many neurological and psychiatric disorders affect the cerebral cortex, and a clearer understanding of the molecular processes underlying human corticogenesis will provide greater insight into such pathologies. To date, knowledge of gene expression changes accompanying corticogenesis is largely based on murine data. Here we present a searchable, comprehensive, temporal gene expression dataset encompassing cerebral cortical development from human embryonic stem cells (hESCs). Using a modified differentiation protocol and RNA-Seq technology with computational analysis, we identified sets of genes and long non-coding RNAs that significantly change during corticogenesis, and those enriched for disease-associations. Numerous alternatively-spliced genes with varying temporal patterns of expression are revealed, including TGIF1, involved in holoprosencephaly and MARK1, involved in autism. We have created a database (http://cortecon.neuralsci.org) that provides online, query-based access to changes in RNA expression and alternatively spliced transcripts during human cortical development. Nine timepoints (days 0,7,12,19,26,33,49,63,77) covering human corticogenesis from embyronic stem cells.
2014-07-01 | E-GEOD-56796 | biostudies-arrayexpress
Project description:In this study, we use deep whole genome transcriptome sequencing to show promoter activity changes during progression from normal prostate cells to advanced prostate disease. We show how androgen signaling and somatic alterations such as loss of the tumor suppressor RB1 or the activation of the ERG oncogene are linked to activity of transcription factors at noncanonical promoters. Alternative promoter usage analysis more accurately reflects changes in TF network during disease progression and in response to therapy. Lastly, we use matched whole genome methylation data to demonstrate a link between methylation and alternative promoter activity, dramatically improving the strength of association between gene expression and methylation data.
| EGAS00001006275 | EGA
Project description:CpG island turnover is associated with evolutionary changes in enhancer activity
| PRJNA963191 | ENA
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