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Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis

ABSTRACT: Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis

PROVIDER: PRJNA704321 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13786100_1.fastq.gz	Fastqsanger.gz
	SRR13786100_2.fastq.gz	Fastqsanger.gz
	SRR13786101_1.fastq.gz	Fastqsanger.gz
	SRR13786101_2.fastq.gz	Fastqsanger.gz
	SRR13769977_1.fastq.gz	Fastqsanger.gz

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Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [scATAC-seq]

Project description:Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [scATAC-seq]

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Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [bulkATAC-seq]

Project description:Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [bulkATAC-seq]

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Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [bulkATAC-seq]

Project description:ATAC-seq of Zeb2 WT and Zeb2 enhancer KO B cells

2021-06-14 | GSE167322 | GEO

Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-06-12 | GSE167330 | GEO

Differential usage of transcriptional repressor Zeb2 enhancers distinguishes adult and embryonic hematopoiesis.

Project description:The transcriptional repressor ZEB2 regulates development of many cell fates among somatic, neural, and hematopoietic lineages, but the basis for its requirement in these diverse lineages is unclear. Here, we identified a 400-basepair (bp) region located 165 kilobases (kb) upstream of the Zeb2 transcriptional start site (TSS) that binds the E proteins at several E-box motifs and was active in hematopoietic lineages. Germline deletion of this 400-bp region (Zeb2Δ-165mice) specifically prevented Zeb2 expression in hematopoietic stem cell (HSC)-derived lineages. Zeb2Δ-165 mice lacked development of plasmacytoid dendritic cells (pDCs), monocytes, and B cells. All macrophages in Zeb2Δ-165 mice were exclusively of embryonic origin. Using single-cell chromatin profiling, we identified a second Zeb2 enhancer located at +164-kb that was selectively active in embryonically derived lineages, but not HSC-derived ones. Thus, Zeb2 expression in adult, but not embryonic, hematopoiesis is selectively controlled by the -165-kb Zeb2 enhancer.

| S-EPMC8282756 | biostudies-literature

Differential usage of Zeb2 enhancer distinguishes adult and embryonic hematopoiesis [scATAC-seq]

Project description:scATAC-seq of myeloid cells

2021-06-14 | GSE167329 | GEO

ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

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TCR-Vγδ usage distinguishes pro- and anti-tumor intestinal γδ T cell subsets

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Loss of ZEB2 in basal breast cancer cells

Project description:Study of loss of ZEB2 in breast cancer cells in vitro and in vivo: gene expression and phenotypic switch to more benign behavior of the cancer cells. Morphological, functional and gene microarray analysis following ZEB2 knockdown in MDAMB231 cells reveals gain of epithelial differentiation, reduction of migration, invasion and metastatic capability. The measurement of ZEB2 transcriptional activity in tumor cells efficiently predicts the probability of breast cancer patient survival. Global gene expression profiles were measured using Affymetrix U133 plus2 microarrays in MDAMB231 cells (control and ZEB2 shRNA and siRNA knockdown cells on plastic)

2016-03-15 | E-GEOD-27966 | biostudies-arrayexpress

Ablation of cDC2 development by triple mutations within the Zeb2 enhancer

Project description:The divergence of the common dendritic cell progenitor (CDP) into the conventional type 1 and type 2 dendritic cell (cDC1 and cDC2, respectively) lineages is poorly understood. Some transcription factors act in the commitment of already specified progenitors-such as BATF3, which stabilizes Irf8 autoactivation at the +32 kb Irf8 enhancer-but the mechanisms controlling the initial divergence of CDPs remain unknown. Here we report the transcriptional basis of CDP divergence and describe the first requirements for pre-cDC2 specification. Genetic epistasis analysis suggested that Nfil3 acts upstream of Id2, Batf3 and Zeb2 in cDC1 development but did not reveal its mechanism or targets. Analysis of newly generated NFIL3 reporter mice showed extremely transient NFIL3 expression during cDC1 specification. CUT&RUN and chromatin immunoprecipitation followed by sequencing identified endogenous NFIL3 binding in the -165 kb Zeb2 enhancer at three sites that also bind the CCAAT-enhancer-binding proteins C/EBPα and C/EBPβ. In vivo mutational analysis using CRISPR-Cas9 targeting showed that these NFIL3-C/EBP sites are functionally redundant, with C/EBPs supporting and NFIL3 repressing Zeb2 expression at these sites. A triple mutation of all three NFIL3-C/EBP sites ablated Zeb2 expression in myeloid, but not lymphoid progenitors, causing the complete loss of pre-cDC2 specification and mature cDC2 development in vivo. These mice did not generate T helper 2 (TH2) cell responses against Heligmosomoides polygyrus infection, consistent with cDC2 supporting TH2 responses to helminths. Thus, CDP divergence into cDC1 or cDC2 is controlled by competition between NFIL3 and C/EBPs at the -165 kb Zeb2 enhancer.

2022-04-19 | GSE188579 | GEO

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