Journal
CELL
Volume 182, Issue 4, Pages 992-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.06.037
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Funding
- NCI Cancer Center Support Grant [P30 CA91842]
- ICTS/CTSA Grant from the National Center for Research Resources (NCRR), a component of the National Institutes of Health (NIH) [UL1 TR000448]
- NIH Roadmap for Medical Research
- Hope Center Viral Vectors Core
- P30 Neuroscience Blueprint Interdisciplinary Center Core award [P30 NS057105]
- NIH [R21 HG009750, R01 GM126112, U01 MH109133, RF1 MH117070, T32 GM007200, T32 HG000045, F30 HG009986, T32 GM008151, F32 NS105363, T32 HL125241, T32 GM007067]
- Children's Discovery Institute [MC-II-2016-533]
- Allen Distinguished Investigator Award (through the Paul G. Allen Frontiers Group)
- Vallee Scholar Award
- Sloan Research Fellowship
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Cellular heterogeneity confounds in situ assays of transcription factor (TF) binding. Single-cell RNA sequencing (scRNA-seq) deconvolves cell types from gene expression, but no technology links cell identity to TF binding sites (TFBS) in those cell types. We present self-reporting transposons (SRTs) and use them in single-cell calling cards (scCC), a novel assay for simultaneously measuring gene expression and mapping TFBS in single cells. The genomic locations of SRTs are recovered from mRNA, and SRTs deposited by exogenous, TF-transposase fusions can be used to map TFBS. We then present scCC, which map SRTs from scRNA-seq libraries, simultaneously identifying cell types and TFBS in those same cells. We benchmark multiple TFs with this technique. Next, we use scCC to discover BRD4-mediated cell-state transitions in K562 cells. Finally, we map BRD4 binding sites in the mouse cortex at single-cell resolution, establishing a new method for studying TF biology in situ.
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