Gene expression profiles of SOX17 overexpression in the KYSE170 luciferase cell
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE35975 | GEO | 2014/02/12
SECONDARY ACCESSION(S): PRJNA151627
REPOSITORIES: GEO
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2014-02-12 | E-GEOD-35975 | biostudies-arrayexpress
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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.
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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 endothelial cells, 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 induced endothelial dysfunctions including upregulation of cell cycle programming and paracrine effect, proliferative and anti-apoptotic phenotypes, impaired cellular junction and BMP signaling. E2F Transcription Factor 1 (E2F1) signaling was showed to mediate the SOX17 deficiency-induced EC dysfunction. Pharmacological inhibition of E2F1 in ecKO Sox17 mice attenuated PH and cell cycle programming. Our study demonstrated that endothelial SOX17 deficiency induces PH through E2F1 and targeting E2F1 signaling represents a promising approach in PAH patients.
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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
Project description:The SOX17 triple-mutant SOX17FNV is a more potent inducer of pluripotency than wild-type SOX2 for unknown features outside its DNA binding high mobility group box domain. Using an inducible reprogramming system, we verified that wild-type SOX17 is not capable to induce pluripotency but SOX17FNV outperforms SOX2 in mouse and human. In mature pluripotent stem cells, SOX17FNV can fully replace SOX2 without compromising self-renewal and pluripotency despite considerable sequence variation. Binding assays using full length proteins expressed in mammalian cells show that SOX17FNV and SOX17 co-bind OCT4 more tightly than SOX2 albeit with switched preferences for composite DNA motifs. Through the systematic analyses of domain deletions, we found that the N-terminus is dispensable for the reprogramming activity of SOX17FNV whilst the C-terminus encodes for essential as well as superfluous domains. Domains have non-additive and partially compensatory effects suggesting that versatile multivalent interaction drive transactivation and reprogramming. We define a minimal SOX17FNV (miniSOX) that can support reprogramming without loss in activity enabling payload reduction within reprogramming cassettes. The definition, functional evaluation and utilisation of potent effector domains that are optimised to pioneer cell fate transition will open up new avenues to enhance cellular reprogramming and stem cell engineering with synthetic transcription factors.
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Project description:The SOX17 triple-mutant SOX17FNV is a more potent inducer of pluripotency than wild-type SOX2 for unknown features outside its DNA binding high mobility group box domain. Using an inducible reprogramming system, we verified that wild-type SOX17 is not capable to induce pluripotency but SOX17FNV outperforms SOX2 in mouse and human. In mature pluripotent stem cells, SOX17FNV can fully replace SOX2 without compromising self-renewal and pluripotency despite considerable sequence variation. Binding assays using full length proteins expressed in mammalian cells show that SOX17FNV and SOX17 co-bind OCT4 more tightly than SOX2 albeit with switched preferences for composite DNA motifs. Through the systematic analyses of domain deletions, we found that the N-terminus is dispensable for the reprogramming activity of SOX17FNV whilst the C-terminus encodes for essential as well as superfluous domains. Domains have non-additive and partially compensatory effects suggesting that versatile multivalent interaction drive transactivation and reprogramming. We define a minimal SOX17FNV (miniSOX) that can support reprogramming without loss in activity enabling payload reduction within reprogramming cassettes. The definition, functional evaluation and utilisation of potent effector domains that are optimised to pioneer cell fate transition will open up new avenues to enhance cellular reprogramming and stem cell engineering with synthetic transcription factors.
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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.
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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. Total RNA were isolated from 5 independent, freshly isolated aliquots of 10,000 HSCs isolated from 8-week old Sox17-transgenic ((tetO)7CMVSox17-IRES-NucEGFP;B6.Cg-Gt(ROSA)26Sortm1(rtTA*M2)Jae/J double transgenic) or littermate control mice that were treated with doxycycline for 5 days to induce transgene expression. Purified RNA was reverse transcribed and amplified using the WT-Ovation™ Pico RNA Amplification system (NuGEN Technologies) following the manufacturer’s instructions. Sense strand cDNA was generated using WT-Ovation™ Exon Module (NuGEN), then fragmented and labeled using the FL-Ovation™ cDNA Biotin Module V2 (NuGEN). 2.5µg of labeled cDNA were hybridized to Affymetrix Mouse Gene ST 1.0 microarrays.
2011-07-14 | E-GEOD-30445 | biostudies-arrayexpress
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.
2011-07-15 | GSE30445 | GEO