Expression data from wild type and Sox17 heterozygous mutant uteri in early pregnancy
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ABSTRACT:
PROVIDER: PRJNA611549 | ENA |
REPOSITORIES: ENA
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Project description:SOX17 activity in the uterine epithelium is essential for the implantation of mouse embryos. Previously, we demonstrated that female Sox17-heterozygous mutant mice are subfertile, and two active copies of Sox17 are required for the proper implantation of mouse embryos. To understand which implantation step is most sensitive to the Sox17 gene dosage, we comprehensively investigated the RNA transcriptomes of Sox17-heterozygous mutant mice.
2020-03-10 | GSE146630 | GEO
Project description:Mammalian embryo development is dependent on the ability of the uterus to allow and support the implantation of the embryo. Here we demonstrate that ablation of Sox17 specifically in the uterine epithelium results in altered uterine epithelial cell proliferation, uterine gland development and embryo implantation. Uteri lacking Sox17 showed reduction in LIF and IHH signaling which are critical for embryo implantation. ChIP-seq analysis demonstrated that SOX17 binds to a region 19kb 5’ to the Ihh locus. In vivo deletion of this enhancer by the CRISPR-Cas technology reduced Ihh expression in uteri and altered proper endometrial epithelial-stromal interactions required for pregnancy leading to compromised fertility. The SOX17 binding peak at 19kb from the Ihh promoter also bound GATA2, FOXA2 and PGR. Bioinformatic analysis of regions overlapping SOX17, GATA2, FOXA2 and PGR bindings shows 737 genes with these common binding sites. This cluster of transcription factors identified in this enhancer region may represent a combination of regulatory elements essential for uterine epithelial gene expression and differentiation.
2018-08-09 | GSE118264 | GEO
Project description:Mammalian embryo development is dependent on the ability of the uterus to allow and support the implantation of the embryo. Here we demonstrate that ablation of Sox17 specifically in the uterine epithelium results in altered uterine epithelial cell proliferation, uterine gland development and embryo implantation. Uteri lacking Sox17 showed reduction in LIF and IHH signaling which are critical for embryo implantation. ChIP-seq analysis demonstrated that SOX17 binds to a region 19kb 5’ to the Ihh locus. In vivo deletion of this enhancer by the CRISPR-Cas technology reduced Ihh expression in uteri and altered proper endometrial epithelial-stromal interactions required for pregnancy leading to compromised fertility. The SOX17 binding peak at 19kb from the Ihh promoter also bound GATA2, FOXA2 and PGR. Bioinformatic analysis of regions overlapping SOX17, GATA2, FOXA2 and PGR bindings shows 737 genes with these common binding sites. This cluster of transcription factors identified in this enhancer region may represent a combination of regulatory elements essential for uterine epithelial gene expression and differentiation.
2018-08-09 | GSE118327 | GEO
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
Project description:Sox17 expression is important for development of gallbladder and bile duct systems in embryo, and it is reported that gallbladder hypoplasia in Sox17 hetero genic embryo. Additionally it was reported that hepatitis was occurred in Sox17 hetero genic newborn by gallbladder hypoplasia. So, we examined Sox17 gene cascade and the role for the formation of gallbladder and bile duct systems by microarray analysis on Sox17 hetero genic gallbladder in day 15 of pregnancy when Sox17 express and gallbladder epithelium alternated morphology. We detected that expression of Sonic hedgehog (shh) signal genes decreased in sox17+/- gallbladder and cysticduct as compared with the wildtype gallbladders.These arry analysis in gallbladder and cysticduct reveal expression of shh in developmental gallbladder is downstream in sox17+/- and gene expression in sox17+/- gallbladder was similar in cysticduct .
2017-05-30 | GSE74576 | GEO
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. Livers were isolated from E12.5 Sox17∆50/∆50 and Sox17+/+ embryos (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.
2024-10-31 | E-MTAB-13982 | biostudies-arrayexpress
Project description:The expression of K-ras transgene is induced in K-rasV12+/-/Cre+/+/ROSA26R-LacZ+/+ transgenic mice uteri, which were primed with hormone treatment. Decidualization was artificially induced in these uteri and hormone injection was withdrawn to induced menstruation-like endometrial degeneration. Microarray was then used to study the molecular changes in these menstruating uteri following the K-ras activation.
2009-04-03 | GSE15518 | GEO
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
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: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