Journal
NATURE COMMUNICATIONS
Volume 12, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-021-26530-2
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Funding
- Interdisciplinary Center for Clinical Research (IZKF) Aachen, RWTH Aachen University Medical School, Aachen, Germany
- Deutsche Forschungsgemeinschaft [DFG-GE 2811/3, DFG SFB/TRR57 P30, SFB/TRR219 P5]
- European Research Council [ERC-StG 677448]
- Bundesministerium fur Bildung und Forschung (BMBF e:Med Consortia Fibromap)
- clinician-scientist program of the German Society of Internal Medicine (DGIM)
- DFG [SFB/TRR 219, P5]
- ITC RWTH Aachen University [rwth0233, rwth0429]
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The authors present a computationally efficient imputation method called scOpen to improve downstream analyses of scATAC-Seq data for identifying transcriptional regulators of kidney fibrosis. scOpen is based on regularized non-negative matrix factorization and effectively addresses the sparsity issue in scATAC-Seq data, demonstrating its power in dissecting regulatory changes in kidney fibrosis development.
scATAC-Seq yields data that is extremely sparse. Here, the authors present a computationally efficient imputation method called scOpen that improves the downstream analyses of scATAC-Seq data and use it to identify transcriptional regulators of kidney fibrosis. A major drawback of single-cell ATAC-seq (scATAC-seq) is its sparsity, i.e., open chromatin regions with no reads due to loss of DNA material during the scATAC-seq protocol. Here, we propose scOpen, a computational method based on regularized non-negative matrix factorization for imputing and quantifying the open chromatin status of regulatory regions from sparse scATAC-seq experiments. We show that scOpen improves crucial downstream analysis steps of scATAC-seq data as clustering, visualization, cis-regulatory DNA interactions, and delineation of regulatory features. We demonstrate the power of scOpen to dissect regulatory changes in the development of fibrosis in the kidney. This identifies a role of Runx1 and target genes by promoting fibroblast to myofibroblast differentiation driving kidney fibrosis.
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