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Sall4 and Gata4 Induce Cardiac Fibroblast Transition Towards a Partially Multipotent State with Cardiogenic Potential

ABSTRACT: Sall4 and Gata4 Induce Cardiac Fibroblast Transition Towards a Partially Multipotent State with Cardiogenic Potential

PROVIDER: PRJNA1119911 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29273100_1.fastq.gz	Fastqsanger.gz
	SRR29273100_2.fastq.gz	Fastqsanger.gz
	SRR29273101_1.fastq.gz	Fastqsanger.gz
	SRR29273101_2.fastq.gz	Fastqsanger.gz
	SRR29273102_1.fastq.gz	Fastqsanger.gz

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Sall4 and Gata4 Induce Cardiac Fibroblast Transition Towards a Partially Multipotent State with Cardiogenic Potential

Project description:Cardiac cellular fate transition holds remarkable promise for the treatment of ischemic heart disease. We report that overexpressing two transcription factors, Sall4 and Gata4, which play distinct and overlapping roles in both pluripotent stem cell reprogramming and embryonic heart development, induces a fraction of stem-like cells in rodent cardiac fibroblasts that develop unlimited ex vivo expandability with clonogenicity. Under suitable conditions, these expanding cells demonstrate a high susceptibility to differentiating into various cardiovascular cell types. RNA-Seq was conducted to elucidate the gene expression profiles in these cells with and without specific differentiation.

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Sall4 regulates distinct transcription circuitries in different blastocyst-derived stem cell lineages

Project description:Stem cells self-renew or differentiate under the governance of a stem cell-specific transcriptional program with each transcription factor orchestrating the activities of a particular set of genes. Here we demonstrate that a single transcription factor is able to regulate distinct core circuitries in two different blastocyst-derived stem cell lines, embryonic stem (ES) and extra-embryonic endoderm (XEN) cells. The transcription factor, Sall4, is required for early embryonic development and for ES cell pluripotency. Sall4 is also expressed in XEN cells and depletion of Sall4 disrupts self-renewal and induces differentiation. Genome-wide analysis reveals Sall4 is regulating different gene sets in ES and XEN cells, and depletion of Sall4 targets in the respective cell types induces differentiation. With Oct4, Sox2 and Nanog, Sall4 forms a crucial interconnected auto-regulatory network in ES cells. In XEN cells, Sall4 regulates key XEN lineageassociated genes, Gata4, Gata6, Sox7 and Sox17. Our findings demonstrate how Sall4 functions as an essential stemness factor for two different stem cell lines. Keywords: ES/XEN comparison, ES Sall4 KD/control KD comparison, and XEN Sall4 KD/control KD comparison

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Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

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A Cdx4-Sall4 regulatory module controls the transition from mesoderm formation to embryonic hematopoiesis

Project description:Deletion of caudal/cdx genes alters hox gene expression and causes defects in posterior tissues and hematopoiesis. Yet, the defects in hox gene expression only partially explain these phenotypes. To gain deeper insight into Cdx4 function, we performed ChIP-seq combined with gene expression profiling in zebrafish, and identified the transcription factor spalt-like 4 (sall4) as a Cdx4 target. ChIP-seq revealed that Sall4 bound to its own gene locus and the cdx4 locus. Expression profiling showed that Cdx4 and Sall4 co-regulate genes such as hox, scl, and lmo2 that initiate hematopoiesis. Combined cdx4/sall4 gene knock-down impairs erythropoiesis, and overexpression of the Cdx4 and Sall4 target genes scl and lmo2 together rescued the erythroid program. These findings suggest that auto- and cross- regulation of Cdx4 and Sall4 establish a stable molecular circuit in mesoderm that facilitates the activation of the blood-specific program as development proceeds. ChIP-seq was performed against Cdx4, Sall4, H3K27ac, and H3K4me3 in bud-stage zebrafish embryos. Input material was sequenced as controls.

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A Cdx4-Sall4 regulatory module controls the transition from mesoderm formation to embryonic hematopoiesis

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The Nuclear Receptor ERR Cooperates with the Cardiogenic Factor GATA4 to Orchestrate Transcriptional Control of Cardiac Maturation

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SALL4 Occupany in mESCs by Cut & Run

Project description:High confidence SALL4 targets were identified in mESCs by performing Cut&Run on SALL4 Flox/Flox and SALL4 -/- cells. We validated a commercially available antibody that specifically recognizes SALL4 protein.

2022-12-08 | GSE203303 | GEO

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Project description:SALL4 is a nuclear factor central to the maintenance of stem cell pluripotency and is a key component in HCC, a malignancy with no effective treatment. In cancer cells, SALL4 associates with NuRD to silence tumor suppressor genes such as PTEN. Here, we design a potent therapeutic SALL4 peptide (FFW) capable of antagonizing the SALL4-NURD interaction using systematic truncation and amino acid substitution studies. To understand the pathways affected by the peptide treatment, we performed RNA sequencing on cells treated with different peptides. Furthermore, to identify SALL4 DNA binding targets, we have performed CRUD-ChIP sequencing with SALL4 and H2K27Ac antibodies on HCC cell line SNU398.

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Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder ES cells were cultured with or without mouse embryonic fibroblast (MEF) feeder cells in LIF-supplemented medium as described. To maintain the expression of Oct3/4, all ES cells were cultured in the presence of Blasticidin. Four samples were analyzed. GSM356329, GSM356330 : cultured in the absence of feeders GSM356331, GSM356332 : cultured on the feeders

2009-04-01 | E-GEOD-14219 | biostudies-arrayexpress

Sall4: -/- NT1 vs TBV

Project description:Sall genes are expressed early in development and in diversity of embryonic and adult structures. Sall4 plays a crucial role during the development of a number of systems. Mutations in the SALL4 gene have been linked to Okihiro/acro-renal-ocular syndrome, in which patients exhibit forearm malformations and eye movement deficits. Homozygote and heterozygote Sall4 cells from mouse blastocysts were collected and used to design a genetrap mouse mutant line. The homozygote Sall4 ES cells form mouse blastocyst were hybridizised versus TBV wildtype cells to detect changes in gene expression. Three biological samples of different passages of the same clone of NT1 and TBV were analyzed in 13 chip hybridizations; each sample was analyzed in 2-5 experimental replicates including dye swap experiments. Keywords: others

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