Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Epigenetic profiles of fate-restricted HSCs [Bulk_ATACseq_HSC]

ABSTRACT: HSC subtypes with distintic lineage restrictions have been previously reported. Here we examine the chromatin landscapes of HSC subtypes with P-restricted, PEM-restricted or multilineage in vivo output.

ORGANISM(S): Mus musculus

PROVIDER: GSE188106 | GEO | 2023/02/22

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiles of fate-restricted HSCs [Bulk RNAseq HSC]

Project description:HSC subtypes with distintic lineage restriction have been previously reported. Here we examine the transcriptome profiles of HSC subtypes with P-restricted, PEM-restricted or multilineage in vivo output.

2023-02-22 | GSE188113 | GEO

Single cell transcriptomics of fate-restricted HSCs [scRNAseq HSC]

Project description:HSC subtypes with distintic lineage restriction have been previously reported. Here we examine the single cell transcriptomics of HSC subtypes with P-restricted, PEM-restricted or multilineage in vivo output.

2023-02-22 | GSE188118 | GEO

fate-restricted HSCs

Project description:fate-restricted HSCs

| PRJNA777793 | ENA

Resolving fate and transcriptome of hematopoietic stem cell clones [multiple cell types]

Project description:Hematopoietic stem cell (HSC) differentiation into mature lineages has been studied under physiological conditions in vivo by genetic barcoding-driven lineage tracing. HSC clones differ in output (differentiation-inactive versus differentiation-active), and in fates (multilineage versus lineage-restricted). Single-cell sequencing data revealed transcriptome diversity of HSC and progenitors, and suggested differentiation pathways. However, molecular hallmarks of functionally distinct HSC clones have not been resolved because existing lineage tracing experiments did not provide transcriptomes, and single cell RNA sequencing lacked information on precursor-product relationships, and hence fate. To close this gap, here we introduce PolyloxExpress, a Cre recombinase-dependent DNA substrate for in situ barcoding in mice that is expressed as mRNA. PolyloxExpress barcoding allows parallel readout of clonal HSC fates (via comparison of barcodes in HSC and mature lineages), and transcriptomes (via single-cell RNA sequencing and barcode matching). Analysing a total of 91 individual HSC clones, we show that differentiation-inactive versus differentiation-active HSC clones reside in different regions of the transcriptional landscape. Inactive HSC clones are closer to the origin of the transcriptional trajectory, yet are proliferatively not more quiescent than active clones. Multilineage versus myelo-erythroid fate-restricted HSC clones show very few transcriptional differences at the HSC stage, yet pronounced fate-specific profiles at the multipotent progenitor stage. Projecting HSC clones with defined fates onto transcriptional landscapes provides a basis for future studies into the molecular determinants for stem cell fate.

2020-08-11 | GSE144273 | GEO

Resolving fate and transcriptome of hematopoietic stem cell clones [LT_ST_HSC]

2020-08-11 | GSE152555 | GEO

Single cell transcriptomics of fate-restricted HSCs [scRNAseq HSC]

Project description:Single cell transcriptomics of fate-restricted HSCs [scRNAseq HSC]

| PRJNA777797 | ENA

Transcription profiles of fate-restricted HSCs [Bulk RNAseq HSC]

Project description:Transcription profiles of fate-restricted HSCs [Bulk RNAseq HSC]

| PRJNA777798 | ENA

HSCs contribute actively to native multilineage hematopoiesis but with reduced differentiation capacity upon aging

Project description:A hallmark of adult hematopoiesis is the continuous replacement of blood cells with limited lifespans. While active hematopoietic stem cell (HSC) contribution to multilineage hematopoiesis is the foundation of clinical HSC transplantation, recent reports have questioned the physiological contribution of HSCs to normal/steady-state adult hematopoiesis. Here, we use inducible lineage tracing from genetically marked adult HSCs and reveal robust HSC-derived multilineage hematopoiesis. This commences via defined progenitor cells, but varies substantially in between different hematopoietic lineages. By contrast, adult HSC contribution to hematopoietic cells with proposed fetal origins is neglible. Finally, we establish that the HSC contribution to multilineage hematopoiesis declines with increasing age. Therefore, while HSCs are active contributors to native adult hematopoiesis, it appears that the numerical increase of HSCs is a physiologically relevant compensatory mechanism to account for their reduced differentiation capacity with age

2018-12-18 | GSE122473 | GEO

Epigenetic profiles of fate-restricted HSCs [Bulk_ATACseq_HSC]

Project description:Epigenetic profiles of fate-restricted HSCs [Bulk_ATACseq_HSC]

| PRJNA777787 | ENA

RNA-seq analysis of EZH1 knockdown in 5F cells, or EZH1 heterozygous and homozygous knockout YS and AGM cells

Project description:Blood develops in distinct stages. Haematopoietic progenitors in the embryo manifest restricted differentiation potential relative to definitive haematopoietic stem cells in adult bone marrow, which support lifelong multilineage haematopoiesis. To identify regulators of embryonic haematopoiesis, we screened chromatin modifiers and identified the Polycomb group protein EZH1 as a barrier to multilineage potential from pluripotent stem cells (PSCs). EZH1 was directly bound to bivalently poised, yet restricted, HSC and lymphoid genes in primitive progenitors; knockdown enabled robust generation of multilineage progenitors. Moreover, EZH1 haploinsufficiency promoted the generation of HSCs with long-term, multilineage and self-renewal potential from sites of embryonic haematopoiesis in vivo. Together, this work identifies EZH1 as a key epigenetic barrier to definitive haematopoiesis during embryonic development, and highlights the utility of chromatin modifiers as cell engineering targets to enhance blood differentiation from PSCs.

2018-01-01 | GSE89415 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data