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A novel lymphoid-primed progenitor marked by Dach1 downregulation identified with single cell multi-omics

ABSTRACT: A novel lymphoid-primed progenitor marked by Dach1 downregulation identified with single cell multi-omics

PROVIDER: PRJNA561654 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10022295_1.fastq.gz	Fastqsanger.gz
	SRR10022295_2.fastq.gz	Fastqsanger.gz
	SRR10022296_1.fastq.gz	Fastqsanger.gz
	SRR10022296_2.fastq.gz	Fastqsanger.gz
	SRR10022297_1.fastq.gz	Fastqsanger.gz

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A novel lymphoid-primed progenitor marked by Dach1 downregulation identified with single cell multi-omics

Project description:A classical view of blood cell development is that multipotent haematopoietic stem and progenitor cells (HSPCs) become lineage-restricted at defined stages. The Lin–c-kit+Sca1+Flt3+ stage, termed lymphoid-primed multipotent progenitors (LMPPs), have lost megakaryocyte and erythroid potential but are heterogeneous in their fate. Through single cell RNA-sequencing, we identify heterogeneous expression of Dach1 and associated genes in this fraction where it co-expressed with myeloid/stem genes but inversely correlated with lymphoid genes. Through generation of Dach1-GFP reporter mice, we identify a transcriptionally and functionally unique Dach1– subpopulation within LMPPs with lymphoid potential but devoid of myeloid potential. We term these ‘lymphoid-primed progenitors’, or LPPs. These findings define the earliest branch point of lymphoid development in haematopoiesis and a means for their prospective isolation.

2019-08-23 | GSE136225 | GEO

Dach1 downregulation marks a lymphoid-primed progenitor in early haematopoiesis (2X96 cells)

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Dach1 downregulation marks a lymphoid-primed progenitor in early haematopoiesis (2X96 cells)

Project description:Dach1 downregulation marks a lymphoid-primed progenitor in early haematopoiesis (2X96 cells)

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DACH1 expression in U87 cells

Project description:Loss or reduction in function of tumor suppressor genes contributes to tumorigenesis. We identified a novel homozygous deletion of DACH1 in gliomas. We generated U87TR-Da glioma cell line, where DACH1 expression could be activated by exposure of cells to doxycycline, and examined changing global gene expression by DACH1 expression. Expression of DACH1 in U87TR-Da cells can be induced by exposure of the cells to doxycycline. We analyzed gene expression profiles of DACH1-induced/repressed U87TR-Da cells. And we also compared gene expression profiles of DACH1-induced/repressed U87TR-Da cells under different culture condition, DMEMF(serum-containing) and NBE(serum-free)

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DACH1 expression in U87 cells

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DACH1 inhibits TGF-beta signaling through binding Smad4

Project description:The vertebrate homologues of Drosophila dachsund, DACH1 and DACH2, have been implicated as important regulatory genes in development. DACH1 plays a role in retinal and pituitary precursor cell proliferation and DACH2 plays a specific role in myogenesis. DACH proteins contain a domain (DS-domain) that is conserved with the proto-oncogenes Ski and Sno. Since the Ski/Sno proto-oncogenes repress AP-1 and SMAD signaling, we hypothesized that DACH1 might play a similar cellular function. Herein, DACH1 was found to be expressed in breast cancer cell lines and to inhibit TGF-beta induced apoptosis. DACH1 repressed TGF-beta induction of AP-1 and Smad signaling in gene reporter assays and repressed endogenous TGF-beta responsive genes by microarray analyses. DACH1 bound to endogenous NCoR and Smad4 in cultured cells and DACH1 co-localized with NCoR in nuclear dot-like structures. NCoR enhanced DACH1 repression and the repression of TGF-beta-induced AP-1 or Smad-signaling by DACH1 required the DACH1 DS domain. The DS-domain of DACH was sufficient for NCoR-binding at a Smad4-binding site. Smad4 was required for DACH1 repression of Smad signaling. In Smad4 null HTB-134 cells, DACH1 inhibited the activation of SBE-4 reporter activity induced by Smad2 or Smad3 only in the presence of Smad4. DACH1 participates in the negative regulation of TGF-beta signaling by interacting with NCoR and Smad4. Keywords: other

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Transcription profiling timecourse of induced DACH1 expression in a human breast cancer cell line

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Single cell analysis of Dach1 overexpressing endothelial cells

Project description:Overexpression of the transcriptional regulator Dach1 can induce coronary artery specification in embryonic mice. Here, we used single cell RNA sequencing to determine how Dach1 overexpression affects global gene expression to causes changes in arterial development. E15.5 control and endothelial specific Dach1 overexpression hearts were collection and FACS sorted to capture endothelial cells. 10x single cell libraries were then created and sequenced using Illumina high throughput sequencing. After identifying differentially expressed genes and assigning the cells to unique clusters, we found that the population of cells collected from Dach1 overexpression mice had a higher percentage of artery cells. Additionally, Dach1 overexpression upregulated the expression of artery genes and downregulated transcripts related to lipid metabolism in select clusters.

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2021-05-19 | GSE168676 | GEO

lncRNA downregulation

Project description:lncRNA downregulation

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