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Embryonic stem cells derived from developmentally incompetent embryos deficient in maternal and zygotic Cdx2

ABSTRACT: Separation of cell lineages during early mammalian development is required to establish the pluripotent founder cell population that will give rise to the embryo proper and a functional trophoblast to support its development. We systemically assessed the role of the homeobox gene Cdx2 in vivo and in vitro development with an RNAi approach. Effective elimination of both maternal and zygotic Cdx2 resulted in typical phenotypes of Cdx2-mutant embryos, such as failure of hatching and implantation. However, the blastulation and expression of TE specific markers in these Cdx2-deficient embryos excluded the possibility of Cdx2 to act as a TE determinant, although compromised structure and functioning of TE was observed and the resulted embryos were not viable. Strikingly, the efficiency of stem cell derivation was significantly higher than control when embryos were put on MEF at the 8-cell stage and the derived stem cells were fully pluripotent as shown by chimera and tetraploid complementation experiments. Comparative genomic hybridization of wild type and Cdx2 mutant at 8-cell and blastocyst mouse embryos were performed.

ORGANISM(S): Mus musculus

PROVIDER: GSE12330 | GEO | 2008/12/30

SECONDARY ACCESSION(S): PRJNA113219

REPOSITORIES: GEO

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Embryonic stem cells derived from developmentally incompetent embryos deficient in maternal and zygotic Cdx2

Project description:Separation of cell lineages during early mammalian development is required to establish the pluripotent founder cell population that will give rise to the embryo proper and a functional trophoblast to support its development. We systemically assessed the role of the homeobox gene Cdx2 in vivo and in vitro development with an RNAi approach. Effective elimination of both maternal and zygotic Cdx2 resulted in typical phenotypes of Cdx2-mutant embryos, such as failure of hatching and implantation. However, the blastulation and expression of TE specific markers in these Cdx2-deficient embryos excluded the possibility of Cdx2 to act as a TE determinant, although compromised structure and functioning of TE was observed and the resulted embryos were not viable. Strikingly, the efficiency of stem cell derivation was significantly higher than control when embryos were put on MEF at the 8-cell stage and the derived stem cells were fully pluripotent as shown by chimera and tetraploid complementation experiments. Comparative genomic hybridization of wild type and Cdx2 mutant at 8-cell and blastocyst mouse embryos were performed. 8-cell biological duplicates and blastocyst stage biological triplicates embryos were used.The hybridization experiments were duplicated in a reciprocal labeling manner to reduce dye integration bias (dye-swaps).

2008-12-29 | E-GEOD-12330 | biostudies-arrayexpress

Functional role of GATA3 and CDX2 in lineage specification during bovine early embryonic development

Project description:Current understandings of the initiation of the trophectoderm (TE) program in mammalian embryonic development lacks evidence of how TE-associated factors such as CDX2 and GATA3 participate in bovine lineage specification. In this study, we describe the effects of TE-associated factors on lineage specification marker genes such as SOX2, OCT4, NANOG, GATA6 and SOX17, assisted by a cytosine base editor system. Interestingly, GATA3 downregulates the NANOG expression in bovine blastocysts. Further analysis of the blastocyst mosaic shows that GATA3 is required for NANOG in TE cells of bovine blastocysts. It is worthy to notice that, unlike mouse embryos where GATA3 and CDX2 did not reciprocally affect each other in bovine embryos.

2022-10-26 | GSE216123 | GEO

CDX2 ChIP-seq

Project description:Somatic DNA alteration underlies tumor development and progression, and gives rise to tumors with diverse genetic contexts. Here, we identify in a collection of 29 colorectal cancer cell lines and 226 primary colorectal tumors recurrent amplification of chromosome 13, an alteration highly restricted to colorectal-derived cancers. A minimal region of amplification on 13q12.2 pinpoints caudal type homeobox transcription factor CDX2, a master regulator of anterior-posterior patterning, midgut development, and intestinal epithelial cell differentiation and maintenance. In contrast to its described role as a colorectal tumor suppressor, we show that in the context of genomic amplification, CDX2 is required for proliferation and anchorage-independent growth of colorectal cancer cells. By genome-wide expression and location analysis, we reveal that CDX2 directly promotes expression of Wnt pathway genes. Further results suggest that CDX2 induces expression of intestinal differentiation markers and modulates Î²-catenin transcriptional activity. These data characterize CDX2 as a novel lineage-survival oncogene deregulated in colorectal cancer. ChIP-seq analysis of CDX2 binding sites in COLO320 cells

2012-11-02 | E-GEOD-30026 | biostudies-arrayexpress

Cdx2 transcription factor binding in intestinal villus and gene expression profiling in Cdx mutant mice

Project description:We conditionally inactivated mouse Cdx2, a dominant regulator of intestinal development, and mapped its genome occupancy in adult intestinal villi. Although homeotic transformation, observed in Cdx2-null embryos, was absent in mutant adults, gene expression and cell morphology were vitally compromised. Lethality was accelerated in mice lacking both Cdx2 and its homolog Cdx1, with exaggeration of defects in crypt cell replication and enterocyte differentiation. Cdx2 occupancy correlated with hundreds of transcripts that fell but not with equal numbers that rose with Cdx loss, indicating a predominantly activating role at intestinal cis-regulatory regions. Integrated consideration of a mutant phenotype and cistrome hence reveals the continued and distinct requirement in adults of a master developmental regulator that activates tissue-specific genes. Cdx2 ChIP-seq in mouse villus, and gene expression data from Cdx1, Cdx2 and compound knockout mouse intestine

2011-04-13 | E-GEOD-24633 | biostudies-arrayexpress

CDX2 ChIP-seq

2012-11-02 | GSE30026 | GEO

Cdx2 transcription factor binding in intestinal villus and gene expression profiling in Cdx mutant mice

2011-04-13 | GSE24633 | GEO

Ectopic expression of the homeobox gene Cdx2 in the epiblast

Project description:This dataset describes the transcriptomic profiling by mRNA-seq of head tissues of E10.5 control or ectopically Cdx2-expressing embryos. Each condition was analyzed in 3 heads to address the role of Cdx2 in embryonic axis determination.

2019-11-04 | GSE123559 | GEO

Cdx2 ChIP-seq performed in E8.5 whole mouse embryos

Project description:We identified genomic regions bound by Cdx2 in E8.5 whole embryos relative to an IgG control.

2019-03-27 | GSE128858 | GEO

CDX2 dose-dependently influences the GRN underlying vascularization in human extraembryonic mesoderm-like cells

Project description:Proper regulation of gene dosage is critical for the development of the early embryo and the extraembryonic tissues that support it. Specifically, loss of Cdx2 in vivo leads to stunted development of the allantois, an extraembryonic mesoderm-derived structure that is critical for nutrient delivery and waste removal in the early embryo. In this study, we investigate how CDX2 dose-dependently influences the gene regulatory network underlying extraembryonic mesoderm development. By generating an allelic series for CDX2 in human induced pluripotent stem cells consisting of WT, heterozygous, and null CDX2 genotypes, differentiating these cells in a 2D gastruloid model, and subjecting these cells to multiomic single nucleus RNA and ATAC sequencing, we identify several genes regulating cytoskeletal integrity, adhesiveness, and polarity of the extraembryonic mesoderm and in a dose-dependent manner, including CDH1 and WNT5B. Despite these dose-dependent gene expression patterns, snATAC-seq reveals that heterozygous CDX2 expression is capable of inducing a WT-like chromatin accessibility profile, suggesting accessibility is not sufficient to drive gene expression when the CDX2 dose is reduced. Finally, because the loss of CDX2 or TBXT phenocopy one another in vivo, we compare differentially expressed genes in our CDX2 knock-out model to those from TBXT knock-out hiPSCs differentiated in an analogous experiment. This comparison identifies several genes critical for cytoskeletal integrity and vasculogenesis, including ANK3 and ANGPT1. Taken together, these results inform how CDX2 dose-dependently regulates gene expression in the extraembryonic mesoderm and suggest these genes may underlie defects in vascular development and allantoic elongation seen in the absence or reduction of CDX2 in vivo.

2024-02-14 | GSE251813 | GEO

Cdx2 Binding Sites On Cdx2 Expressing ES Cells

Project description:A) Chromatins were prepared from Cdx2-inducible ES cells cultured for 48 - 60 hours in the Dox+ and Dox- conditions. Chromatin immunoprecipitation (ChIP) was carried out by using anti-FLAG M2 affinity gel. ChIP product was tested by Western blotting using anti-FLAG antibody. Nuclear extract from ES cells cultured for 48 - 60 hours in Dox+ and Dox- condition was used for the Western blot. B) CDX2 ChIP-Seq peaks in the Hoxa7 gene region. UCSC Mouse Mm9 browser view of Hoxa7 gene locus after mapping CDX2 ChIP-Seq tags locations in the wiggle format. CDX2 ChIP-Seq peaks are shown in red color. C) Cdx2 ChIP-Seq result was verified by qPCR. Target genes were indicated in (G). Primers flanking a promoter region of Hbb-b1 and Pou5f1 as well as a gene desert region in chromosome 3 were used as negative controls. Primers flanking of Actb gene promoter were used for normalization. The relative enrichment of CDX2 binding was indicated as fold change. (D) CDX2-binding motifs identified with CisFinder using 200 bp sequences centered at ChIP sites. (F) Potential CDX2-direct target genes based on ChIP-Seq and the alteration of expression by Cdx2-overexpression. (G) Identification of CDX2 target genes by combining information on binding sites with gene expression response to Cdx2 over-expression

2009-10-01 | GSE14586 | GEO

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