Expression data from wild type and Sox17 heterozygous mutant uteri in early pregnancy
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA611549 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:In addition to accumulation of step-wise genetic mutations, epigenetic alterations play critical roles in the evolution of colon cancers. However, distinct mutational patterns and patient backgrounds render it challenging to distinguish driver epigenetic alterations from passenger epigenetic alterations. To address this, we combined the colon cancer organoid orthotopic transplantation approach with comprehensive epigenomic and transcriptomic analyses. We found that an in vivo environment induces epigenetic alterations with fetal intestinal features that converge on SOX17, a transcription factor that is required for endoderm development. Surprisingly, SOX17 knockout leads to tumour rejection in immunocompetent mice, but not in immunodeficient mice, by turning immune cold tumours into hot with robust infiltration of activated CD8+ T cells. Mechanistically, SOX17 suppresses Ifngr1-mediated MHC-I expression to evade CD8+ T cell-mediated tumour cell killing. At the tumour initiation, SOX17 expression is induced by APC loss, and SOX17 facilitates the production of LGR5- cells with low MHC-I expression to evade immune surveillance. Together, our result reveals that SOX17 is a master transcriptional factor that induces in vivo epigenetic reprograming of tumours, which provides fundamental understanding of how an immune evasion program is initiated at the early stages of colon cancer development.
2024-02-28 | GSE222710 | GEO
Project description:In addition to accumulation of step-wise genetic mutations, epigenetic alterations play critical roles in the evolution of colon cancers. However, distinct mutational patterns and patient backgrounds render it challenging to distinguish driver epigenetic alterations from passenger epigenetic alterations. To address this, we combined the colon cancer organoid orthotopic transplantation approach with comprehensive epigenomic and transcriptomic analyses. We found that an in vivo environment induces epigenetic alterations with fetal intestinal features that converge on SOX17, a transcription factor that is required for endoderm development. Surprisingly, SOX17 knockout leads to tumour rejection in immunocompetent mice, but not in immunodeficient mice, by turning immune cold tumours into hot with robust infiltration of activated CD8+ T cells. Mechanistically, SOX17 suppresses Ifngr1-mediated MHC-I expression to evade CD8+ T cell-mediated tumour cell killing. At the tumour initiation, SOX17 expression is induced by APC loss, and SOX17 facilitates the production of LGR5- cells with low MHC-I expression to evade immune surveillance. Together, our result reveals that SOX17 is a master transcriptional factor that induces in vivo epigenetic reprograming of tumours, which provides fundamental understanding of how an immune evasion program is initiated at the early stages of colon cancer development.
2024-02-28 | GSE222709 | GEO
Project description:In addition to accumulation of step-wise genetic mutations, epigenetic alterations play critical roles in the evolution of colon cancers. However, distinct mutational patterns and patient backgrounds render it challenging to distinguish driver epigenetic alterations from passenger epigenetic alterations. To address this, we combined the colon cancer organoid orthotopic transplantation approach with comprehensive epigenomic and transcriptomic analyses. We found that an in vivo environment induces epigenetic alterations with fetal intestinal features that converge on SOX17, a transcription factor that is required for endoderm development. Surprisingly, SOX17 knockout leads to tumour rejection in immunocompetent mice, but not in immunodeficient mice, by turning immune cold tumours into hot with robust infiltration of activated CD8+ T cells. Mechanistically, SOX17 suppresses Ifngr1-mediated MHC-I expression to evade CD8+ T cell-mediated tumour cell killing. At the tumour initiation, SOX17 expression is induced by APC loss, and SOX17 facilitates the production of LGR5- cells with low MHC-I expression to evade immune surveillance. Together, our result reveals that SOX17 is a master transcriptional factor that induces in vivo epigenetic reprograming of tumours, which provides fundamental understanding of how an immune evasion program is initiated at the early stages of colon cancer development.
2024-02-28 | GSE245668 | 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:In addition to accumulation of step-wise genetic mutations, epigenetic alterations play critical roles in the evolution of colon cancers. However, distinct mutational patterns and patient backgrounds render it challenging to distinguish driver epigenetic alterations from passenger epigenetic alterations. To address this, we combined the colon cancer organoid orthotopic transplantation approach with comprehensive epigenomic and transcriptomic analyses. We found that an in vivo environment induces epigenetic alterations with fetal intestinal features that converge on SOX17, a transcription factor that is required for endoderm development. Surprisingly, SOX17 knockout leads to tumour rejection in immunocompetent mice, but not in immunodeficient mice, by turning immune cold tumours into hot with robust infiltration of activated CD8+ T cells. Mechanistically, SOX17 suppresses Ifngr1-mediated MHC-I expression to evade CD8+ T cell-mediated tumour cell killing. At the tumour initiation, SOX17 expression is induced by APC loss, and SOX17 facilitates the production of LGR5- cells with low MHC-I expression to evade immune surveillance. Together, our result reveals that SOX17 is a master transcriptional factor that induces in vivo epigenetic reprograming of tumours, which provides fundamental understanding of how an immune evasion program is initiated at the early stages of colon cancer development.
2024-02-28 | GSE222712 | GEO