98%
921
2 minutes
20
EpiScanpy is a toolkit for the analysis of single-cell epigenomic data, namely single-cell DNA methylation and single-cell ATAC-seq data. To address the modality specific challenges from epigenomics data, epiScanpy quantifies the epigenome using multiple feature space constructions and builds a nearest neighbour graph using epigenomic distance between cells. EpiScanpy makes the many existing scRNA-seq workflows from scanpy available to large-scale single-cell data from other -omics modalities, including methods for common clustering, dimension reduction, cell type identification and trajectory learning techniques, as well as an atlas integration tool for scATAC-seq datasets. The toolkit also features numerous useful downstream functions, such as differential methylation and differential openness calling, mapping epigenomic features of interest to their nearest gene, or constructing gene activity matrices using chromatin openness. We successfully benchmark epiScanpy against other scATAC-seq analysis tools and show its outperformance at discriminating cell types.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8410937 | PMC |
http://dx.doi.org/10.1038/s41467-021-25131-3 | DOI Listing |
BMB Rep
September 2025
Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Korea.
DNA, a large molecule located in the nucleus, carries essential genetic information, including gene loci and cis-regulatory elements. Despite its extensive length, DNA is compactly stored within the limited space of the nucleus due to its hierarchical three-dimensional (3D) organization. In this structure, DNA is organized into territories known as topologically associated domains (TADs).
View Article and Find Full Text PDFSemin Hematol
August 2025
Division of Stem Cells and Cancer, German Cancer Research Center (DKFZ) and DKFZ-ZMBH Alliance, Heidelberg, Germany; Heidelberg Institute for Stem Cell Technology and Experimental Medicine (HI-STEM, gGmbH), Heidelberg, Germany.
Acute myeloid leukemia (AML) is an aggressive blood cancer in which disease initiation and relapse are driven by leukemic cells with stem-like properties, known as leukemic stem cells (LSCs). The LSC compartment is highly heterogenous and this contributes to differences in therapy response. This heterogeneity is determined by genetic and nongenetic factors including somatic mutations, the cell of origin, transcriptional and epigenetic states as well as phenotypic plasticity.
View Article and Find Full Text PDFCurr Opin Plant Biol
September 2025
State Key Laboratory of Gene Function and Modulation Research, Beijing Advanced Center of RNA Biology (BEACON), School of Advanced Agricultural Sciences, Peking University, 100871, Beijing, China. Electronic address:
Plants exhibit remarkable regenerative capacities, enabling tissue repair, de novo organogenesis, and somatic embryogenesis in response to mechanical injury or phytohormone induction. At the cellular level, this process is driven by the establishment of pluripotency and cell fate specification, regulated through dynamic epigenomic remodeling. Emerging studies have begun to unravel the intricate regulatory circuits governing regeneration in a cell-type- and lineage-specific manner.
View Article and Find Full Text PDFMedComm (2020)
September 2025
Somatic retinoblastoma 1 () loss is prevalent across different cancer types and is enriched in treatment-refractory tumors, such as castration-resistant prostate cancer (CRPC) and small-cell lung cancer, but cannot be considered as a direct druggable target. In this study, we revealed that the close proximity of nudix hydrolase 15 () and may result in their common somatic codeletion or epigenomic cosilencing in different cancer types and subsequent significant positive correlations of their expressions at the bulk transcriptional and single-cell levels. With clinical CRPC samples, co-loss of and were commonly observed (14 out of 21).
View Article and Find Full Text PDFAging increases the global burden of disease, yet its molecular basis remains incompletely understood. Recent studies indicate that reversible epigenetic drift-spanning DNA methylation clocks, histone codes, three-dimensional chromatin, and noncoding RNA networks-constitutes a central regulator of organismal decline and age-related diseases. How these epigenetic layers interact across different tissues-and how best to translate them into therapeutic strategies-are still open questions.
View Article and Find Full Text PDF