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Removing an acid residue is necessary and sufficient to turn SOX17 into a pluripotency factor

ABSTRACT: Removing an acid residue is necessary and sufficient to turn SOX17 into a pluripotency factor

PROVIDER: PRJNA1073433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27871923_1.fastq.gz	Fastqsanger.gz
	SRR27871923_2.fastq.gz	Fastqsanger.gz
	SRR27871924_1.fastq.gz	Fastqsanger.gz
	SRR27871924_2.fastq.gz	Fastqsanger.gz
	SRR27871925_1.fastq.gz	Fastqsanger.gz

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Removing an acid residue is necessary and sufficient to turn SOX17 into a pluripotency factor

Project description:SOX17 directs the differentiation of the extraembryonic endoderm and acts as a human germline specifier. The replacement of an acidic residue at position 57 with a basic residue found in SOX2 turns SOX17 into a pluripotency factor. Here we systematically interrogated how mutations at this critical position affect the cellular reprogramming activity of SOX17. We found that most mutations turn SOX17 into a pluripotency factor regardless of their biophysical properties. The mutation to an aspartate allows the SOX17E57D protein to maintain a self-renewing endodermal state. Only the glutamate found in the wild-type protein can effectively block a SOX17/OCT4 dimer from binding composite DNA elements found in pluripotency enhancers. Insights into how modifications of an ultra-conserved residue affect functions of developmental transcription factor provide avenues to advance cell fate engineering.

2024-02-10 | GSE255055 | 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

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

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.

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Sox17-transgenic hematopoietic stem cell microarray

Project description:The transcription factor SOX17 is expressed by fetal, but not adult hematoipoietic stem cells (HSCs), and is required for the maintenance of fetal and neonatal, but not adult, HSCs. In the current study we show that ectopic expression of Sox17 in adult HSCs and transiently reconstituting multipotent progenitors was sufficient to confer increased self-renewal potential and the expression of fetal HSC genes including fetal HSC surface markers. To assess the acute effects of ectopic Sox17 expression on global gene expression in adult HSCs, we performed microarray analysis to compare the gene expression profile of adult Sox17-trangenic and control HSCs after short induction of Sox17-transgene expression.

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Transcriptional regulation of Sox17 in HUVEC

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Whole transcriptome analysis of Sox17.Epi and Endo cells in mouse embryos

Project description:This experiment has been done to understand the dynamics of gene expression in Sox17.Epi and Endo cells using multiplex RNA-Seq technology. Sox17.Epi (Sox17^GFP+EpCAM+) and Sox17.Endo (Sox17^GFP+EpCAM-) cells were isolated by FACS from E9.5 mouse embryos. The spatial comparison between Sox17.Epi versus Sox17.Endo provides insight into which genes are differentially of specifically expressed in two populations.

2012-07-20 | E-MTAB-970 | biostudies-arrayexpress

Effect of Rad6 backside beta-turn mutations

Project description:Effect of Rad6 backside beta-turn mutations

| PRJNA580524 | ENA