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Developmental trajectory of pre-hematopoietic stem cell formation from endothelium (scRNA-seq data set)

ABSTRACT: Developmental trajectory of pre-hematopoietic stem cell formation from endothelium (scRNA-seq data set)

PROVIDER: PRJNA564578 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10087300.fastq.gz	Fastqsanger.gz
	SRR10087301.fastq.gz	Fastqsanger.gz
	SRR10087302.fastq.gz	Fastqsanger.gz
	SRR10087303.fastq.gz	Fastqsanger.gz
	SRR10087304.fastq.gz	Fastqsanger.gz

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Developmental trajectory of pre-hematopoietic stem cell formation from endothelium

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Developmental trajectory of pre-hematopoietic stem cell formation from endothelium (scRNA-seq data set)

Project description:To examine the cell and molecular transitions between endothelial (E), hemogenic endothelial (HE), and intra-arterial clusters (IAC) cells, and the heterogeneity of hematopoietic stem and progenitor cells (HSPCs) within the IACs, we profiled ~40,000 cells from the caudal arteries (dorsal aorta, umbilical, vitelline arteries) of embryonic day (E) 9.5 to 11.5 mouse embryos by single-cell RNA sequencing (scRNA-Seq). We identified a developmental bottleneck in endothelial to hematopoietic transition (EHT) and heterogeneity within the IAC population.

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Project description:To examine the cell and molecular transitions between endothelial (E), hemogenic endothelial (HE), and intra-arterial clusters (IAC) cells, we profiled ~1700 cells from the caudal arteries (dorsal aorta, umbilical, vitelline) of embryonic day (E) 10.5 mouse embryos by single-cell ATAC sequencing (scATAC-Seq). We found extensive cis--regulatory landscape change during the endothelial to hematopoietic transition (EHT).

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Developmental trajectory of pre-hematopoietic stem cell formation from endothelium

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Project description:Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow are derived from a small population of hemogenic endothelial (HE) cells located in the major arteries of the mammalian embryo. HE cells undergo an endothelial to hematopoietic cell transition, giving rise to HSPCs that accumulate in intra-arterial clusters (IAC) before colonizing the fetal liver. To examine the cell and molecular transitions between endothelial (E), HE, and IAC cells, and the heterogeneity of HSPCs within IACs, we profiled ∼40 000 cells from the caudal arteries (dorsal aorta, umbilical, vitelline) of 9.5 days post coitus (dpc) to 11.5 dpc mouse embryos by single-cell RNA sequencing and single-cell assay for transposase-accessible chromatin sequencing. We identified a continuous developmental trajectory from E to HE to IAC cells, with identifiable intermediate stages. The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs. A developmental bottleneck separates pre-HE from HE, with RUNX1 dosage regulating the efficiency of the pre-HE to HE transition. A distal candidate Runx1 enhancer exhibits high chromatin accessibility specifically in pre-HE cells at the bottleneck, but loses accessibility thereafter. Distinct developmental trajectories within IAC cells result in 2 populations of CD45+ HSPCs; an initial wave of lymphomyeloid-biased progenitors, followed by precursors of hematopoietic stem cells (pre-HSCs). This multiomics single-cell atlas significantly expands our understanding of pre-HSC ontogeny.

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Project description:Across species, hematopoietic stem and progenitor cells (HSPCs) arise during embryogenesis from a specialized arterial population, termed hemogenic endothelium. Here, we describe a mechanistic role for the epigenetic regulator, Enhancer of zeste homolog-1 (Ezh1) in vertebrate HSPC production via regulation of hemogenic commitment. Loss of ezh1 in zebrafish embryos favored acquisition of hemogenic (gata2b) and HSPC (runx1) fate at the expense of the arterial program (ephrinb2a, dll4). In contrast, ezh1 overexpression blocked hematopoietic progression via maintenance of arterial gene expression. The related polycomb group subunit, Ezh2, functioned in a non-redundant, sequential manner, whereby inhibition had no impact on arterial identity, but was capable of blocking ezh1-knockdown associated HSPC expansion. Single-cell RNA-seq across ezh1 genotypes revealed a dropout of ezh1+/- cells among arterial endothelium associated with positive regulation of gene transcription. Exploitation of Ezh1/2 modulation has potential functional relevance for improving in vitro HSPC differentiation from induced pluripotent stem cell sources.

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