Isopoda
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA389401 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5666735_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR5666736_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR5666737_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR5666738_subreads.fastq.gz | Fastqsanger.gz |
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Project description:Mitochondrial heteroplasmy, the presence of more than one mtDNA variant in a cell or individual is not as uncommon as previously thought. It is mostly due to the high mutation rate of the mtDNA and limited repair mechanisms present in the mitochondrion. The phenomenon has been studied mostly in human samples and in medical contexts. Heteroplasmy has also been researched in other species in fields such as forensics or genetic foot printing, but these studies usually focused on contained families within closely related species. Here we describe a large cross-species evaluation of heteroplasmy in mammals. We employed a novel approach to detect mitochondrial heteroplasmy in both novel and previously reported ChIP-sequencing datasets, which include concomitant mitochondrial DNA sequenced in the experiment. Here, we report novel ChIP-seq experiments for H3K4me1 and CEBPA across mammals, as well as some H3K4me3, H3K27ac and total histone H3 experiments. Most of the reported CEBPA experiments are good quality pull-downs, however the quality of many of the other experiments reported here has not been interrogated in detail. Whereas this does not affect the investigation of mitochondrial DNA pollution for the purposes of this study, both H3K4me1 and total histone H3 ChIP-seq datasets were often sequenced to relatively low depth and showed low ChIP enrichment compared to the other antibodies.
2016-05-13 | E-MTAB-3933 | biostudies-arrayexpress
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE148508 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE142743 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE142742 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE142741 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE142740 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE148509 | GEO
Project description:Natural mitochondrial DNA (mtDNA) sequence variation plays a fundamental role in human disease and enables the clonal tracing of native human cells. While various genotyping approaches revealed mutational heterogeneity in human tissues and single cells, current methodologies are limited by scale. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell Assay for Transposase Accessible Chromatin with sequencing (mtscATAC-seq) protocol and computational framework that facilitate high-confidence mtDNA mutation calling in thousands of single cells. Further, the concomitant high-quality accessible chromatin readout enables the paired inference of individual cell mtDNA heteroplasmy, clonal lineage, cell state, and accessible chromatin regulatory features. Our multi-omic analyses reveals single-cell variation in heteroplasmy of a pathologic mtDNA variant (m.8344A>G), which we tie to intra-individual chromatin variability and clonal evolution. Further, using somatic mtDNA mutations, we clonally trace thousands of hematopoietic cells in vitro and in patients with chronic lymphocytic leukemia, linking epigenomic variability to subclonal evolution in vivo.
2020-07-13 | GSE142744 | GEO
Project description:Mitochondria generate signals of adaptation that regulate nuclear genes expression via retrograde signaling. But this phenomenon is complexified when qualitatively different mitochondria and mitochondrial DNA (mtDNA) coexist within cells. Although this cellular state of heteroplasmy leads to divergent phenotypes clinically, its consequences on cellular function and the cellular transcriptome are unknown. To interrogate this phenomenon, we generated somatic cell cybrids harboring increasing levels of a common mtDNA mutation (tRNALeu(UUR) 3243A>G) and mapped the resulting cellular phenotypes and transcriptional profiles across the complete range of heteroplasmy. Small increases in mutant mtDNAs caused relatively modest defect in mitochondrial oxidative capacity, but resulted in sharp transitions in mitochondrial ultrastructure and in the nuclear and mitochondrial transcriptomes, with the critical functional threshold corresponding to the induction of epigenetic regulatory systems. Principal component analysis underscores how each heteroplasmy level occupies a different "transcriptional space", with low levels heteroplasmy (20-30%) producing a dose-response linear progression in one direction, and mutationload of 50, 60 and 90% producing changes in the opposite direction. Hence, subtle changes in mitochondrial energetics can act through the epigenome to generate the phenotypes of the common “complex” diseases. Cells were generated by transferring the wildtype (3243A) and mutant (3243G) mtDNAs from a heteroplasmic 3243A>G patient’s lymphoblastoid cell line into 143B(TK-) mtDNA-deficient (ρo) cells and selected for transmitochondrial cybrids. Subsequent mtDNA depletion, reamplification, and cloning (Wiseman and Attardi, 1978) resulted in a series of stable cybrids harboring approximately 0, 20, 30, 50, 60, 90, and 100% 3243G mutant mtDNAs. Total RNA extracted from each cell line was then extracted, depleted of rRNA, and measured in sequenced in triplicates.
2014-09-02 | E-GEOD-56158 | biostudies-arrayexpress