Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1212703 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A Single-Cell Atlas of In Vivo Mammalian Chromatin Accessibility
| PRJNA437471 | ENA
Project description:Technical advances have enabled the collection of genome and transcriptome data sets with single-cell resolution. However, single-cell characterization of the epigenome has remained challenging. Furthermore, because cells must be physically separated prior to biochemical processing, conventional single-cell preparatory methods scale linearly. We applied combinatorial cellular indexing to measure chromatin accessibility in thousands of single cells per assay, circumventing the need for compartmentalization of individual cells. We report chromatin accessibility profiles from over 15,000 single cells and use these data to cluster cells on the basis of chromatin accessibility landscapes. We identify modules of coordinately regulated chromatin accessibility at the level of single cells both between and within cell types, with a scalable method that may accelerate progress toward a human cell atlas. 3 replicates from GM12878 and HL-60 cell lines collected for differential gene expression analysis.
2015-05-07 | E-GEOD-68102 | biostudies-arrayexpress
Project description:A single-cell atlas of chromatin accessibility in mouse organogenesis
| PRJNA893359 | ENA
Project description:Single-cell chromatin accessibility atlas of human retinal organoid development
| PRJEB60385 | ENA
Project description:A single-cell atlas of chromatin accessibility in the human genome
| PRJNA764714 | ENA
Project description:A number of studies have reported cell heterogeneity within the developing mouse pancreas, as well as the transcriptional profiles corresponding to various cell states. The upstream mechanisms that initiate and maintain gene expression programs across cell states, however, remain largely unknown. Here, we applied single-nucleus ATAC-Seq to developing mouse pancreas to generate an atlas of chromatin accessibility, at single-cell resolution. Our goals were first, to generate an atlas of chromatin accessibility of embryonic mouse pancreas, at single-cell resolution, that can serve as a resource for the field. We aimed to provide such a resource not only for epithelial cells within the pancreas, but for non-epithelial (e.g., mesenchymal) as well. Our second goal was to identify gene regulatory networks governing cell fate transitions through integration of single-cell chromatin accessibility and gene expression data.
2023-05-18 | GSE210569 | GEO
Project description:Recent surveys of mouse organogenesis cell atlas (MOCA) with single cell transcriptomics have uncovered hundreds of cell types, but the cell-type-specific transcriptional regulatory programs responsible for the unique identity and function of each cell type have yet to be elucidated. We applied a four-level combinatorial indexing assay, SPATAC-seq, to profile the chromatin accessibility in >350,000 cells derived from 13 embryos staged between embryonic day (E) 10.5 and 13.5 in a single experiment. The resulting map revealed the status of open chromatin for 844,817 candidate cis-regulatory elements (cCREs) in 33 main cell types and 296 subtypes. By integrating this accessible chromatin atlas with scRNA data of MOCA, we characterized the gene regulatory sequences and transcription factors associated with cell fate commitment, such as unreported role of Nr5a2 and Gata6 in gastrointestinal tract. Finaly, we integrated this atlas with previous scATAC-seq data from mouse embryos at E8.25 and 13 adult mouse tissues to dissect life stage specific gene regulatory programs across different cell types. This rich resource and comprerhensive analysis provide a foundation for expolring gene regulators in mammalian cell differentiation.
2024-04-14 | GSE216371 | GEO
Project description:We performed single nucleus ATAC (snATAC-seq) to generate cell-type-specific chromatin accessibility atlas of the mouse kidneys with ischemia-reperfusion injury. The single nucleus RNA-seq of the same samples were previously published (GEO139107)
2024-07-31 | GSE252105 | GEO
Project description:Aging leads to functional decline across tissues, often accompanied by profound changes in cellular composition and cell-intrinsic molecular states. However, a comprehensive catalog of how the population of individual cell types change with age and the associated epigenomic dynamics is lacking. Here, we constructed a single-cell chromatin accessibility atlas consisting of ~7 million cells from 21 tissue types spanning three age groups in both sexes. This dataset revealed 536 main cell types and 1,828 finer‐grained subtypes, defined by unique chromatin accessibility landscapes at ~1.3 million cis‐regulatory elements. We observed widespread remodeling of immune lineages, with increases in plasma cells and macrophages, and depletion of T and B cell progenitors. Additionally, non-immune cell populations, including kidney podocytes, ovary granulosa cells, muscle tenocytes and lung aerocytes, showed marked reductions with age. Meanwhile, many subtypes changed synchronously across multiple organs, underscoring the potential influence of systemic inflammatory signals or hormonal cues. At the molecular level, aging was marked by thousands of differentially accessible regions, with the most concordant changes shared across cell types linked to genes related to inflammation or development. Putative upstream factors, such as intrinsic shifts in transcription factor usages and extrinsic cytokine signatures, were identified. Notably, around 40% of aging‐associated main cell types and subtypes showed sex‐dependent differences, with tens of thousands of chromatin accessibility peaks altered exclusively in one sex. Together, these findings present a comprehensive framework of how aging reshapes the chromatin landscape and cellular composition across diverse tissues, offering a comprehensive resource for understanding the molecular and cellular programs underlying aging and supporting the exploration of targeted therapeutic strategies to address age-related dysfunction.
2025-05-15 | GSE288730 | GEO