A single cell atlas of gene regulatory elements in the human heart
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PROVIDER: PRJNA671259 | ENA |
REPOSITORIES: ENA
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Project description:In this work we present atlas of human cardiac regulatory elements defined by CAGE (cap analysis of gene expression) technique. The dataset includes right and left atria and ventricles form both healthy and failing samples. The deep sequencing of CAGE libraries on Illumina HiSeq2500, mapping, and signal clustering resulted in identification of 65,458 CAGE peaks, from which 55,204 were robust decomposition peak identifiers (DPIs) and 10,254 bidirectional enhancers. We created comprehensive classification of the peaks by applying machine learning along with annotation from available databases containing cardiac data. Identified CAGE peaks were arranged into non-overlapping 400 bp consensus clusters. Our classification method determined 17,668 promoters and 14,920 enhancers active in the human heart. Differential expression analysis revealed regulatory elements activated or inactivated in healthy or failing states. About 10% of heart related GWAS SNPs were found to be located around heart CAGE clusters. The library of cardiac promoters and enhancers is available in Zenbu reports for browsing and visualization. Superior and inferior sinoatrial node samples are labeled as sSAN and iSAN, respectively.
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2022-12-01 | E-MTAB-8826 | biostudies-arrayexpress
Project description:Cis-regulatory elements (CREs) encode the genomic blueprints for coordinating the spatiotemporal regulation of gene transcription programs necessary for highly specialized cellular functions. To identify cis-regulatory elements underlying cell-type specification and developmental transitions, we implemented single-cell sequencing of Assay for Transposase Accessible Chromatin (scATAC-seq) in an atlas of Zea mays tissues and organs. We describe 92 distinct patterns of chromatin accessibility across more than 165,913 putative CREs, greater than 56,575 cells, and 52 known cell-types using a novel regularized quasibinomial logistic model for estimating single cell accessibility. Cell-type specification could be largely explained by combinatorial accessibility of transcription factors (TFs) and their associated binding. Analysis of cell type-specific co-accessible chromatin recapitulated higher-order chromatin interactions, providing novel insight into cell type-specific regulatory dynamics. Integration of genetic diversity data revealed cell-type specific CREs contributed to specific morphological and molecular phenotypic traits indicative of their cellular functions, expanding our understanding of the molecular influence of complex traits in a eukaryotic species.
2020-09-30 | GSE155178 | GEO
Project description:BACKGROUND: Alternative splicing plays crucial roles in normal heart development and cardiac disease by influencing protein-coding sequences, functional domains, and molecular networks. However, a detailed characterization of the human heart isoform landscape remains incomplete. METHODS: Leveraging long-read single-nucleus RNA sequencing and computational analysis, we dissected full-length isoform heterogeneities, expression patterns, and usage shifts across cell types, cell states, and cardiac conditions of the adult left ventricle. We applied in silico approaches to assess the functional relevance of identified isoforms; validated isoform compositions of representative cardiac genes using reverse transcription quantitative polymerase chain reaction and targeted amplicon sequencing; and developed a web server for interactive navigation of our results. RESULTS: The data revealed that isoform heterogeneity is widespread in the cardiac cellular system, serving as a posttranscriptional buffer system that calibrates the molecule reservoirs in human hearts. In healthy left ventricles, ≈30% of cell type–specific genes were polyform, using multiple isoforms tailored to cell type–specific programs. Among ubiquitously expressed genes, >300 showed differential isoform usage with cell type specificity. Compared with heart failure, 379 genes in cardiomyocytes demonstrated marked isoform usage shifts, most of which are predicted to change protein coding outcomes through direct changes in protein coding sequences and switches between intron retention and non–protein-coding biotypes. In contrast, cell state–specific programs tend to operate on monoform genes associated with changes among cell states. In addition, our data revealed heart failure–associated differential isoform usage events in stromal and immune cell types in the cardiac microenvironment. CONCLUSIONS: We present a comprehensive atlas of splicing isoforms in the normal adult heart and heart failure through long-read single-nucleus RNA sequencing and comprehensive computational analyses. The results suggest crucial roles of isoforms in buffering core cellular programs and contributing to disease-associated cell states. The full-length details of these cell-specific isoforms serve as an important reference for downstream translational and mechanistic studies and are available on our online data portal at https://github.com/gaolabtools/heart-isoform-atlas. Github repo: https://github.com/gaolabtools/heart-isoform-atlas doi: 10.1161/CIRCULATIONAHA.125.074959
2025-09-29 | GSE288222 | GEO
Project description:Through integrated H2BGFP ChIP-seq data over multiple conditions and time points, as well as other related ChIP-seq and RNA-seq data in adult mouse heart. We observed genomewide and locus-specific H2B turnover in non-proliferating adult cardiomyocytes (Cms), and a majority of genomic regions with rapid turnover rates distributes on cis-regulatory elements, as well as these regions are associated with heart function, regulatory factors binding and their activities. Moreover, H2B turnover rate is always positively correlated with gene transcription level on enhancers, promoters and exons. The rapid turnover rates at cis-regulatory elements can be partially explained by the binding and co-binding of RNAP II and various transcription factors (TFs). Our further analysis revealed that not only rapid H2B turnover at cis-regulatory elements responses to heart disease, but also slow turnover at H3K27me3 sites functionally responses to heart disease with a different manner. More generally, we indicate that the binding and co-binding of DNA-binding proteins, such as TFs and epigenetic enzymes, all of them coupled with H2B turnover to modulate gene transcription and chromatin state.
2020-04-17 | GSE97876 | GEO
Project description:We used ATLAS-seq to comprehensively map the genomic location of LINE-1 elements belonging to the youngest and potentially polymorphic subfamily (L1HS-Ta). This was performed in single-cells of 2 preimplantation embryos (E3 and E6) as well as from the remaining inner cell mass (denoted T). In brief, single cells were isolated from the inner cell mass of preimplantation embryos by laser drilling and micromanipulation. Whole-genome Multiple Displacement Amplification was performed on each isolated single cells, as well as on the remaining cells of the inner cell mass as a population (samples labelled 'T'). Then we applied ATLAS-seq to map L1HS-Ta retrotransposons. This approach relies on the random mechanical fragmentation of the genomic DNA to ensure high-coverage, ligation of adapter sequences, suppression PCR-amplification of L1HS-Ta element junctions, and Ion Torrent sequencing using single-end 400 bp read chemistry. A notable aspect of ATLAS-seq is that we can obtain both L1 downstream and upstream junctions (3'- and 5'-ATLAS-seq libraries, respectively), for full-length L1 elements.
2023-09-30 | E-MTAB-8616 | biostudies-arrayexpress