Effects of the Sox17∆50 mutation on SOX17 function in mouse embryonic biliary development
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB74552 | ENA |
REPOSITORIES: ENA
Similar Datasets
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: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: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:Effects of the Sox17 ∆50 mutation on SOX17 function in mouse embryonic liver development
| PRJEB74456 | ENA
Project description:Effects of the Sox17∆50/GFP mutation on SOX17 function in mouse embryonic liver development
| PRJEB74458 | ENA
Project description:To determine the role of specific cis-regulatory elements within the Sox17 endoderm-preferential TSS2 promoter, we generated Sox17mut5 mutant animals and surveyed how this mutation altered Sox17 expression. Gallbladders were isolated from P21 Sox17mut5/mut5 and Sox17+/+ (n = 4 of each genotype), RNA isolated, and bulk RNA-Seq performed.
2024-10-31 | E-MTAB-13978 | biostudies-arrayexpress
Project description:Effects of the Sox17mut5 mutation on SOX17 function in mouse embryonic gallbladder development
| PRJEB74445 | ENA
Project description:Background and aims: Cholangiocarcinoma (CCA) is a heterogeneous group of malignancies with features of biliary tract differentiation. Incidence is increasing worldwide and these cancers collectively represent the second most common primary liver tumour. CCAs are characterized by genetic and epigenetic alterations that determine their pathogenesis. Hypermethylation of the SOX17 promoter was recently reported in human CCA tumours. SOX17 seems to be a key transcription factor for biliary embryogenesis. Here, we evaluated the role of SOX17 in cholangiocyte differentiation and in cholangiocarcinogenesis. Methods: SOX17 expression and function was evaluated during the differentiation of human induced pluripotent stem cells (iPSC) into cholangiocytes, in the dedifferentiation of normal human cholangiocytes (NHC) and in cholangiocarcinogenesis. Lentiviruses overexpressing or knocking-down SOX17 (Lent-SOX17 and Lent-shRNA-SOX17, respectively) were used. Gene expression arrays were performed. Results: SOX17 expression is highly induced in the later stages of cholangiocyte differentiation from iPSC, and mediates the acquisition of the biliary markers cytokeratin (CK) 7 and 19, as well as fibronectin. In addition, SOX17 becomes progressively downregulated in NHC over serial cell passages in vitro and this event is associated with cellular senescence; however, experimental SOX17 knocking-down in differentiated NHC decreased the expression of both CK7 and 19 without affecting cellular senescence. SOX17 expression is reduced in CCA cells compared to NHC, as well as in human CCA tissue compared to human gallbladder tissue or NHC. In a murine xenograft model, overexpression of SOX17 in CCA cells decreased their tumorigenic capacity related to increased oxidative stress and apoptosis. Interestingly, overexpression of SOX17 in NHC did not affect their survival. Moreover, SOX17 overexpression inhibited the Wnt/β-catenin-dependent proliferation in CCA cells and was associated with upregulation of biliary epithelial markers and restoration of the primary cilium length. Both Wnt3a and TGFβ1 decreased SOX17 expression in NHC in a DNMT1-dependent manner. Inhibition of DNMT1 in CCA cells with siRNAs or pharmacological drugs upregulated SOX17 expression. Conclusion: SOX17 regulates the cholangiocyte phenotype and becomes epigenetically downregulated in CCA. SOX17 acts as a tumour suppressor in CCA, and restoration of its expression may have important therapeutic value.
2017-08-31 | GSE77984 | GEO
Project description:To determine the effect of Sox17 overexpression in mouse embryonic stem (ES) cells, we performed gain-of-function analysis by generating ES cell lines carrying a doxycycline inducible FLAG-tagged Sox17 transgene. We treated Sox17-inducible ES cells with doxycycline, collected RNA and performed genome-wide transcriptional analysis. We found that genes invovled in adhesion function and basement membrane establishment were transcriptionally upregulated in ES cells upon induction of Sox17. We also observed downregulation in the transcription of genes involved in pathways known to be functionally important for ES cell pluripotency and self-renewal. However, Sox17 expression was not sufficient to rapidly down-regulate Sox2, Nanog, and Oct4. Two independent doxycycline inducible Sox17-overexpressing mouse embryonic stem cells were derived. The genes expression changes in the Sox17-induced cells were compared to untreated (no doxycycline) controls and to control cells treated with or without doxycycline. The total RNA from these samples were amplified using Ambion Illumina TotalPrep RNA Amplification kit and arrayed on Illumina MouseRef8 v2 chips.
2010-03-31 | E-GEOD-19028 | biostudies-arrayexpress
Project description:To determine the effect of Sox17 overexpression in mouse embryonic stem (ES) cells, we performed gain-of-function analysis by generating ES cell lines carrying a doxycycline inducible FLAG-tagged Sox17 transgene. We treated Sox17-inducible ES cells with doxycycline, collected RNA and performed genome-wide transcriptional analysis. We found that genes invovled in adhesion function and basement membrane establishment were transcriptionally upregulated in ES cells upon induction of Sox17. We also observed downregulation in the transcription of genes involved in pathways known to be functionally important for ES cell pluripotency and self-renewal. However, Sox17 expression was not sufficient to rapidly down-regulate Sox2, Nanog, and Oct4.
2010-03-31 | GSE19028 | GEO