Gata6 induced XEN-like cells w/o Sox7
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE66971 | GEO | 2015/09/14
SECONDARY ACCESSION(S): PRJNA278525
REPOSITORIES: GEO
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Project description:To understand the role of Sox7 in primitive endoderm differentiation, we compare the gene expression pattern of Sox7 (+/-) and Sox7 (-/-) ES cells with or without dexamethasome (Dex) treatment. Because these ES cells harbour Gata6-GR transgene, Dex treatment forces ES cells differentate into XEN-like cells. As Sox7 (-/-) ES cells can differentiate into XEN-like cell by morphology, we assessed genome wide gene expression pattern. Sox7 (+/-) ES cells and Sox7 (-/-) ES cells are forced to differentiate into XEN-like cells by Gata6-GR transgene. To compare the gene expression, we collected RNA samples at day4 with or without dexamethasone treatment from each genotype.
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Project description:The conventional trophoblast stem cells represent post-implantation extraembryonic ectoderm-like state and not that of pre-implantation trophectoderm, irrespective of their origin. To capture the trophectoderm-like state we established culture conditions that facilitate the co-existence of characteristics of both the extraembryonic lineages, namely, primitive endoderm and trophectoderm. We term these cells XTE cells. We carried out RNA-seq on XTE cells from different origins, as well as XEN cells, XEN-like cells, and ES cells, to assess their transcriptional profiles and identify putative marker genes and master regulators.
2022-09-13 | E-MTAB-8788 | biostudies-arrayexpress
Project description:Stem cells self-renew or differentiate under the governance of a stem cell-specific transcriptional program with each transcription factor orchestrating the activities of a particular set of genes. Here we demonstrate that a single transcription factor is able to regulate distinct core circuitries in two different blastocyst-derived stem cell lines, embryonic stem (ES) and extra-embryonic endoderm (XEN) cells. The transcription factor, Sall4, is required for early embryonic development and for ES cell pluripotency. Sall4 is also expressed in XEN cells and depletion of Sall4 disrupts self-renewal and induces differentiation. Genome-wide analysis reveals Sall4 is regulating different gene sets in ES and XEN cells, and depletion of Sall4 targets in the respective cell types induces differentiation. With Oct4, Sox2 and Nanog, Sall4 forms a crucial interconnected auto-regulatory network in ES cells. In XEN cells, Sall4 regulates key XEN lineageassociated genes, Gata4, Gata6, Sox7 and Sox17. Our findings demonstrate how Sall4 functions as an essential stemness factor for two different stem cell lines. Keywords: ES/XEN comparison, ES Sall4 KD/control KD comparison, and XEN Sall4 KD/control KD comparison
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Project description:Specification of the mesodermal lineages requires a complex set of morphogenetic events orchestrated by interconnected signaling pathways and gene regulatory networks. The transcription factor Sox7 has critical functions in differentiation of multiple mesodermal lineages, including cardiac, endothelial, and hematopoietic. Using a doxycycline-inducible mouse embryonic stem cell (mESC) line, we have previously shown that expression of Sox7 in cardiovascular progenitor cells promotes expansion of endothelial progenitor cells. Here, we show that the ability of Sox7 to promote endothelial cell fate occurs at the expense of the cardiac lineage. Using ChIP-Seq coupled with ATAC-Seq we identify downstream target genes of Sox7 in cardiovascular progenitor cells and, by integrating these data with transcriptomic analyses, we define Sox7-dependent gene programs specific to cardiac and endothelial progenitor cells. Further, we demonstrate a protein-protein interaction between SOX7 and GATA4 and provide evidence that Sox7 interferes with the transcriptional activity of Gata4 on cardiac genes. In addition, we show Sox7 modulates WNT and BMP signaling during cardiovascular differentiation. Our data represent the first genome-wide analysis of Sox7 function and reveal a critical role for Sox7 in regulating signaling pathways that affect cardiovascular progenitor cell differentiation.
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Project description:As a transcription factor, SOX7 suppresses cancer development. However, only a few genes were demonstrated as SOX7-activated targets in cancer-irrelevant contexts. We used microarray chips to determine SOX7 target genes in breast cancer cells and discovered multiple signaling pathways altered by ectopic SOX7. We also investigated several genes for their roles in SOX7-mediated tumor suppression. Our study innovatively revealed SOX7 target gene profile in a cancer-relevant context and identified several SOX7-repressed target genes.
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