In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA)
Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome.
Specimen part
View SamplesIn vitro cultured CD34+ derived erythroblasts were sorted using surface markers and processed using RNA-seq Overall design: Biological replicates (3 or 4 per population) were processed across 2-3 biological donors for 8 sorted populations for RNA-seq
Transcriptional States and Chromatin Accessibility Underlying Human Erythropoiesis.
Subject
View SamplesHUDEP-2 cells were lentivirally infected with CRISPRi constructs using a nontargeting guide or guides targeting an enhancer in the TMCC2 locus Overall design: Whole transcriptome libraries were sequenced for three replicates of non-targeting gRNA and two replicates each for two different gRNA targeting a regulatory region upstream of the TMCC2 erythroid-specific isoform
Transcriptional States and Chromatin Accessibility Underlying Human Erythropoiesis.
Cell line, Subject
View SamplesLineage tracing provides unprecedented insights into the fate of individual cells and their progeny in complex organisms. While effective genetic approaches have been developed in vitro and in animal models, these cannot be used to interrogate human physiology in vivo. Instead, naturally occurring somatic mutations have been utilized to infer clonality and lineal relationships between cells in human tissues, but current approaches are limited by high error rates and scale, and provide little information about the state or function of the cells. Here, we show how somatic mutations in mitochondrial DNA (mtDNA) can be tracked by current single cell RNA-Seq (scRNA-Seq) or single cell ATAC-Seq (scATAC-Seq) for simultaneous analysis of single cell lineage and state. We leverage somatic mtDNA mutations as natural genetic barcodes and demonstrate their use as clonal markers to infer lineal relationships. We trace the lineage of human cells by somatic mtDNA mutations in a native context both in vitro and in vivo, and relate it to expression profiles and chromatin accessibility. Our approach should allow lineage tracing at a 100- to 1,000-fold greater scale than with single cell whole genome sequencing, while providing information on cell state, opening the way to chart detailed cell lineage and fate maps in human health and disease. Overall design: A population of 25 transfected TF1 cells were expanded and forwarded to a combination of 1) ATAC-seq and single cell RNA-seq. The single-cell RNA-seq data are listed here. Meta data includes heteroplasmic variant information per cell as well as the group assigned based on the lentiviral barcoding
Lineage Tracing in Humans Enabled by Mitochondrial Mutations and Single-Cell Genomics.
No sample metadata fields
View SamplesLineage tracing provides unprecedented insights into the fate of individual cells and their progeny in complex organisms. While effective genetic approaches have been developed in vitro and in animal models, these cannot be used to interrogate human physiology in vivo. Instead, naturally occurring somatic mutations have been utilized to infer clonality and lineal relationships between cells in human tissues, but current approaches are limited by high error rates and scale, and provide little information about the state or function of the cells. Here, we show how somatic mutations in mitochondrial DNA (mtDNA) can be tracked by current single cell RNA-Seq (scRNA-Seq) or single cell ATAC-Seq (scATAC-Seq) for simultaneous analysis of single cell lineage and state. We leverage somatic mtDNA mutations as natural genetic barcodes and demonstrate their use as clonal markers to infer lineal relationships. We trace the lineage of human cells by somatic mtDNA mutations in a native context both in vitro and in vivo, and relate it to expression profiles and chromatin accessibility. Our approach should allow lineage tracing at a 100- to 1,000-fold greater scale than with single cell whole genome sequencing, while providing information on cell state, opening the way to chart detailed cell lineage and fate maps in human health and disease. A variety of experimental designs using cells derived from both in vitro and in vivo to determine the efficacy of using mtDNA mutations in human clonal tracing. Overall design: A population of 30 primary hematopoietic cells were expanded and forwarded to a combination of ATAC-seq and single cell RNA-seq. single cell RNA-seq samples are listed here.
Lineage Tracing in Humans Enabled by Mitochondrial Mutations and Single-Cell Genomics.
No sample metadata fields
View SamplesLineage tracing provides unprecedented insights into the fate of individual cells and their progeny in complex organisms. While effective genetic approaches have been developed in vitro and in animal models, these cannot be used to interrogate human physiology in vivo. Instead, naturally occurring somatic mutations have been utilized to infer clonality and lineal relationships between cells in human tissues, but current approaches are limited by high error rates and scale, and provide little information about the state or function of the cells. Here, we show how somatic mutations in mitochondrial DNA (mtDNA) can be tracked by current single cell RNA-Seq (scRNA-Seq) or single cell ATAC-Seq (scATAC-Seq) for simultaneous analysis of single cell lineage and state. We leverage somatic mtDNA mutations as natural genetic barcodes and demonstrate their use as clonal markers to infer lineal relationships. We trace the lineage of human cells by somatic mtDNA mutations in a native context both in vitro and in vivo, and relate it to expression profiles and chromatin accessibility. Our approach should allow lineage tracing at a 100- to 1,000-fold greater scale than with single cell whole genome sequencing, while providing information on cell state, opening the way to chart detailed cell lineage and fate maps in human health and disease. A variety of experimental designs using cells derived from both in vitro and in vivo to determine the efficacy of using mtDNA mutations in human clonal tracing. Overall design: Individually sorted cells from clonally derived TF1 clones (C9, D6, and G10) were processed with single cell RNA-seq (Smart-seq2)
Lineage Tracing in Humans Enabled by Mitochondrial Mutations and Single-Cell Genomics.
Specimen part, Cell line, Subject
View SamplesLineage tracing provides unprecedented insights into the fate of individual cells and their progeny in complex organisms. While effective genetic approaches have been developed in vitro and in animal models, these cannot be used to interrogate human physiology in vivo. Instead, naturally occurring somatic mutations have been utilized to infer clonality and lineal relationships between cells in human tissues, but current approaches are limited by high error rates and scale, and provide little information about the state or function of the cells. Here, we show how somatic mutations in mitochondrial DNA (mtDNA) can be tracked by current single cell RNA-Seq (scRNA-Seq) or single cell ATAC-Seq (scATAC-Seq) for simultaneous analysis of single cell lineage and state. We leverage somatic mtDNA mutations as natural genetic barcodes and demonstrate their use as clonal markers to infer lineal relationships. We trace the lineage of human cells by somatic mtDNA mutations in a native context both in vitro and in vivo, and relate it to expression profiles and chromatin accessibility. Our approach should allow lineage tracing at a 100- to 1,000-fold greater scale than with single cell whole genome sequencing, while providing information on cell state, opening the way to chart detailed cell lineage and fate maps in human health and disease. A variety of experimental designs using cells derived from both in vitro and in vivo to determine the efficacy of using mtDNA mutations in human clonal tracing. Overall design: Cells from 3 separate TF1 clones (C9, D6, and G10) were processed with bulk RNA-seq (Smart-seq2)
Lineage Tracing in Humans Enabled by Mitochondrial Mutations and Single-Cell Genomics.
Specimen part, Cell line, Subject
View SamplesThe cytokine interleukin-12 (IL-12) is known to play a central role in adaptive and innate immunity.
Tpl2 kinase regulates T cell interferon-gamma production and host resistance to Toxoplasma gondii.
Sex
View Samples