Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Chemicals orchestrate reprogramming with hierarchical activation of master transcription factors primed by endogenous Sox17 activation

ABSTRACT: Chemicals orchestrate reprogramming with hierarchical activation of master transcription factors primed by endogenous Sox17 activation

PROVIDER: PRJNA602743 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10954114_1.fastq.gz	Fastqsanger.gz
	SRR10954114_2.fastq.gz	Fastqsanger.gz
	SRR10954115_1.fastq.gz	Fastqsanger.gz
	SRR10954115_2.fastq.gz	Fastqsanger.gz
	SRR10954116_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Chemicals orchestrate reprogramming with hierarchical activation of master transcription factors primed by endogenous Sox17 activation

Project description:Mouse somatic cells can be chemically reprogrammed into pluripotent stem cells (CiPSCs) through an intermediate extraembryonic endoderm (XEN)-like state. However, it is elusive how the chemicals orchestrate the cell fate alteration. In this study, we analyze molecular dynamics in chemical reprogramming from fibroblasts to a XEN-like state. We find that Sox17 is initially activated by the chemical cocktails, and XEN cell fate specialization is subsequently mediated by Sox17 activated expression of other XEN master genes, such as Sall4 and Gata4. Furthermore, this stepwise process is differentially regulated. The core reprogramming chemicals CHIR99021, 616452 and Forskolin are all necessary for Sox17 activation, while differently required for Gata4 and Sall4 expression. The addition of chemical boosters in different phases further improves the generation efficiency of XEN-like cells. Taken together, our work demonstrates that chemical reprogramming is regulated in 3 distinct “prime–specify–transit” phases initiated with endogenous Sox17 activation, providing a new framework to understand cell fate determination.

2020-11-05 | GSE144097 | GEO

Chemicals orchestrate reprogramming with hierarchical activation of master transcription factors primed by endogenous Sox17 activation.

Project description:Mouse somatic cells can be chemically reprogrammed into pluripotent stem cells (CiPSCs) through an intermediate extraembryonic endoderm (XEN)-like state. However, it is elusive how the chemicals orchestrate the cell fate alteration. In this study, we analyze molecular dynamics in chemical reprogramming from fibroblasts to a XEN-like state. We find that Sox17 is initially activated by the chemical cocktails, and XEN cell fate specialization is subsequently mediated by Sox17 activated expression of other XEN master genes, such as Sall4 and Gata4. Furthermore, this stepwise process is differentially regulated. The core reprogramming chemicals CHIR99021, 616452 and Forskolin are all necessary for Sox17 activation, while differently required for Gata4 and Sall4 expression. The addition of chemical boosters in different phases further improves the generation efficiency of XEN-like cells. Taken together, our work demonstrates that chemical reprogramming is regulated in 3 distinct "prime-specify-transit" phases initiated with endogenous Sox17 activation, providing a new framework to understand cell fate determination.

| S-EPMC7603307 | biostudies-literature

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

Project description:SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVEC), there is a significant downregulation of SOX17 expression. We hypothesized that SOX17 deficiency contributes to the pathogenesis of PAH and found that mice with endothelial specific disruption (ecKO Sox17) developed spontaneous pulmonary hypertension (PH) and exacerbated hypoxia-induced PH. Loss of SOX17 in lung ECs induces cell cycle programming, proliferative and anti-apoptotic phenotypes, a process mediated by the activation of E2F Transcription Factor 1 (E2F1) signaling. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH and targeting E2F1 signaling represents a promising approach in PAH patients.

2023-03-15 | GSE192649 | GEO

Effects of the Sox17 ∆50 mutation on SOX17 function in mouse embryonic liver development

2024-10-31 | E-MTAB-13982 | biostudies-arrayexpress

Effects of the Sox17∆50/GFP mutation on SOX17 function in mouse embryonic liver development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals, crossed them to a Sox17GFPCre (a Sox17 null allele), and surveyed how this mutation affected Sox17 expression. Livers were isolated from E12.5 Sox17∆50/GFPCRe compound heterozygous and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.

2024-10-31 | E-MTAB-13983 | biostudies-arrayexpress

Effects of the Sox17∆50 mutation on SOX17 function in mouse embryonic biliary development

Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17∆50 mutant animals and surveyed how this mutation altered Sox17 expression. EPCAM+/CXCR4+ endodermal cells were isolated from E10.5 Sox17∆50/∆50 and Sox17+/+ embryos (n = 1 of each genotype). Posterior foregut and midgut regions of embryos were dissected by removal of embryonic head, heart, tail, limb buds, posterior and dorsal body trunk. Sox17+/+ and Sox17Δ50/Δ50 cell samples were labelled with barcodes from 3'CellPlex Kit (10X Genomics) and subsequently pooled together for single isolation, library preparation and sequencing.

2024-10-31 | E-MTAB-14000 | biostudies-arrayexpress

Profiling of melocular mechanism of SOX17 effect during hematopoieisis of human ES cells

Project description:Here, using SOX17-knockout and SOX17-inducible human PSCs, paired with cell biology and molecular profiling studies, we revealed that SOX17 represents a critical upstream factor that is required for activation and linkage of HOXA and arterial programs in hemogenic endothelium and establishing definitive lympho-myeloid hematopoiesis. These SOX17 effects are mediated through activation of NOTCH, CDX2 and retinoic acid signaling. Collectively, these findings are important to design strategies for direct HSC fate programming from hPSCs.

2021-01-06 | GSE140341 | GEO

Transcriptional regulation of Sox17 in HUVEC

Project description:We identified Sox17 as a novel angiogenic transcription factor in the context of tumor. Our data revealed that Sox17 promotes tumor angiogenesis and tumor vessel abnormality. We found that Sox17 is specifically expressed in tumor endothelial cells within tumors. Our study elucidates a novel transcriptional regulation for tumor angiogenesis Control HUVECs vs. Sox17 knockdown HUVECs. Biological replicates: 3 control replicates, 3 transfected replicates.

2012-12-17 | E-GEOD-37395 | biostudies-arrayexpress

Single-cell RNA sequencing on the testis from the rete testis-specific Sox17 conditioinal knockout (cKO) mice and the controls at P14.

Project description:In mammalian testes, a valve-like structure called Sertoli valve is located at the border region of the seminiferous tubule and the rete testis. Having identified Sox17 in the rete testis as a positive regulator of the valve formation, this study aim to elucidate the mechanism of Sox17-expressing rete testis to modulate the testicular homeostasis. Our scRNA-seq data demonstrate the altered gene expression levels of several growth factors in Sox17-depleted rate testis epithelia, and highlighted the altered proportion of Sertoli cells located around the proximal part of the testis. This study provides a comprehensive profile of the proximal part of the testis including the rete testis and Sertoli valve for the first time, and further illustrate the functional role of the Sox17+ rete tesits to orchestrate the testicular homeostasis.

2022-11-27 | GSE190043 | GEO

Transcription profiling of Xenopus laevis early embryos to investigate the roles of Nodal, Mixer and Sox17 in endoderm formation

Project description:A conserved molecular pathway has emerged controlling endoderm formation in Xenopus zebrafish and mice. Key genes in this pathway include Nodal ligands and transcription factors of the Mix-like paired homeodomain class, Gata4-6 zinc finger factors and Sox17 HMG domain proteins. While a linear epistatic pathway has been proposed, the precise hierarchical relationships between these factors and their downstream targets are largely unresolved. Here we used a combination of microarray analysis and loss-of-function experiments to examine the global regulatory network controlling Xenopus endoderm formation. We identified over 300 transcripts enriched in the gastrula endoderm, including most of the known endoderm regulators as well as over a hundred uncharacterized genes. Surprisingly only 10% of the endoderm transcriptome is regulated as predicted by the current linear model. We find that Nodals, Mixer and Sox17 have both shared and distinct sets of downstream targets and that a number of unexpected autoregulatory loops exist between Sox17 and Gata4-6, Sox17 and Bix1, 2, 4 and between Sox17 and Xnr4. We find that Mixer does not function primarily via Sox17 as previously proposed. This data provides a new insight into the complexity of endoderm formation and will serve as valuable resource for establishing a complete endoderm gene regulatory network. Experiment Overall Design: Define a set of transcripts with enriched expression in the gastrula endoderm of the Xenopus laevis embryo and determine how these are regulated by nodal signaling, Mixer and Sox17 using loss-of-function experiments. For more specific details see Sinner et al., (2006) Global analysis of the transcriptional network controlling Xenopus endoderm formation.

2007-10-05 | E-GEOD-4448 | biostudies-arrayexpress

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