Similar Datasets
Project description:BS-seq of Tet-TKD 2-cell embryos
| PRJNA656300 | ENA
Project description:To isolate cell-autonomous effects of TET loss during gastrulation, we utilized a chimeric embryo platform in which fluorescently tagged Tet-deficient and control mouse embryonic stem cells (mESCs) were either injected into tetraploid (4N) or diploid (2N) blastocysts, and allowed to develop in utero. In 4N complemented embryos, the resulting embryonic compartment is solely comprised of the injected mESCs derivatives (hereinafter denoted as whole-embryo chimera), whereas in chimeras obtained using 2N host blastocysts, the embryonic compartment contains both wild-type (WT) and injected cell derivatives (hereinafter denoted as mixed chimera). We performed single-cell RNA-seq for each whole-embryo and mixed chimera embryo, and compared the transcriptomes to a defined single-cell/single-embryo atlas. We further performed methylation analysis using post-bisulfite adaptor tagging (PBAT) for sorted Tet-TKO mutant and control from E8.5 mixed chimeras. Our work demonstrates an unbiased approach for defining intrinsic and extrinsic embryonic gene function based on temporal differentiation atlases, and disentangles the intracellular effects of the demethylation machinery from its broader tissue-level ramifications.
2022-06-14 | GSE205917 | GEO
Project description:The tumorigenesis capacity of MLL-AF4 alone is insufficient for causing leukemia. Based on the finding that an Flt3 gene mutation in the tyrosine kinase domain (TKD) was observed in approximately 15% of MLL leukemia, we investigated synergistic leukemogenesis effects of the two genes in vitro. In a mouse IL3-dependent cell line, 32Dc, the expression of MLL-AF4 and Flt3 TKD was induced using a lentiviral vector. We performed gene expression profiling in the MLL-AF4 and the Flt3 TKD+MLL-AF4 expressing 32Dc cells. The enhancement of Hox genes expression was not identified. However, instead, the expression of S100A6, which was involved in the control of cell proliferation, was synergistically enhanced in the presence of both MLL-AF4 and Flt3 TKD genes. We performed gene expression profiling: 32Dc vs. MLL-AF4 expressing 32Dc, 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc, and MLL-AF4 expressing 32Dc vs. Flt3 TKD+MLL-AF4 expressing 32Dc. A single sample for each expressing cells was analyzed.
2009-03-31 | E-GEOD-14236 | biostudies-arrayexpress
Project description:We sequenced cDNA prepared from ribosomal RNA depleted total RNA of 10-10 embryos co-injected with TBP-,TBP2- and TLF-AS antisense oligonucleotides and with water to create expression profiles of triple knockdown of TBP/TBP-related factors (TKD) and control, respectively, in Xenopus laevis at early developmental stage 10.5. (according to Nieuwkoop and Faber). We executed differential expression analysis of sequence count data (DEseq).
2016-03-07 | GSE76994 | GEO
Project description:To explore the effects of Tet on porcine pre-implantation embryogenesis, we utilized Bobcat339, a specific small-molecule inhibitor of the Tet protein, to treat parthenogenetic 4-cell stage embryos.
2023-12-30 | GSE218707 | GEO
Project description:To determine the transcriptional effects of lack of Tet proteins during early embryogenesis, we performed single-embryo RNA-sequencing of control and TKO embryos (E6.75; 4 embryos from each group). Genome-wide analyses showed that Tet deficiency promotes the expression of mesoderm-related genes during early embryogenesis in vivo.
2016-11-21 | GSE89313 | GEO
Project description:The Ten-eleven translocation (TET) family of dioxygenases can mediate cytosine demethylation by catalyzing the oxidation of 5-methylcytosine (5mC). TET-mediated DNA demethylation controls the proper differentiation of embryonic stem cells and TET proteins display functional redundancy during early gastrulation. However, it is unclear if TET proteins have functional significance in mammalian skeletal development. Here, we report that Tet deficiency in mesoderm mesenchymal stem cells results in severe defects of bone development. The existence of any single Tet gene allele can support early bone formation, suggesting a potential functional redundancy of TET proteins. Integrative analyses of RNA-seq, Whole Genome Bisulfite Sequencing (WGBS) and Assay for Transposase-Accessible Chromatin (ATAC-seq) demonstrate that TET-mediated demethylation increases the chromatin accessibility of target genes by RUNX2 and facilities RUNX2-regulated transcription. In addition, TET proteins interact with RUNX2 through their catalytic domain to regulate cytosine methylation around RUNX2 binding region. The catalytic domain is indispensable for TET proteins to regulate RUNX2 transcription activity on its target genes and to regulate bone development. These results demonstrate that TET proteins function redundantly to regulate RUNX2 activity via dual mechanisms and maintain skeletal homeostasis.
2023-02-28 | GSE167172 | GEO
Project description:Nucleosome occupancy and positioning were examined in foregut stage to compare control and FOXA-TKD using high/low MNase-seq
2024-01-10 | GSE247785 | GEO
Project description:The Ten-eleven translocation (TET) family of dioxygenases can mediate cytosine demethylation by catalyzing the oxidation of 5-methylcytosine (5mC). TET-mediated DNA demethylation controls the proper differentiation of embryonic stem cells and TET proteins display functional redundancy during early gastrulation. However, it is unclear if TET proteins have functional significance in mammalian skeletal development. Here, we report that Tet deficiency in mesoderm mesenchymal stem cells results in severe defects of bone development. The existence of any single Tet gene allele can support early bone formation, suggesting a potential functional redundancy of TET proteins. Integrative analyses of RNA-seq, Whole Genome Bisulfite Sequencing (WGBS) and Assay for Transposase-Accessible Chromatin (ATAC-seq) demonstrate that TET-mediated demethylation increases the chromatin accessibility of target genes by RUNX2 and facilities RUNX2-regulated transcription. In addition, TET proteins interact with RUNX2 through their catalytic domain to regulate cytosine methylation around RUNX2 binding region. The catalytic domain is indispensable for TET proteins to regulate RUNX2 transcription activity on its target genes and to regulate bone development. These results demonstrate that TET proteins function redundantly to regulate RUNX2 activity via dual mechanisms and maintain skeletal homeostasis.
2022-07-07 | GSE174047 | GEO
Project description:The tumorigenesis capacity of MLL-AF4 alone is insufficient for causing leukemia. Based on the finding that an Flt3 gene mutation in the tyrosine kinase domain (TKD) was observed in approximately 15% of MLL leukemia, we investigated synergistic leukemogenesis effects of the two genes in vitro. In a mouse IL3-dependent cell line, 32Dc, the expression of MLL-AF4 and Flt3 TKD was induced using a lentiviral vector. We performed gene expression profiling in the MLL-AF4 and the Flt3 TKD+MLL-AF4 expressing 32Dc cells. The enhancement of Hox genes expression was not identified. However, instead, the expression of S100A6, which was involved in the control of cell proliferation, was synergistically enhanced in the presence of both MLL-AF4 and Flt3 TKD genes.
2009-03-31 | GSE14236 | GEO