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SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [ChIP-seq]

ABSTRACT: SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [ChIP-seq]

PROVIDER: PRJNA485190 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7662166.fastq.gz	Fastqsanger.gz

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SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [array]

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

SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [ChIP-seq]

2018-08-09 | GSE118327 | GEO

SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh

Project description:SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh

| PRJNA485189 | ENA

SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [array]

Project description:SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh [array]

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SOX17 regulates uterine epithelial-stromal cross-talk acting via a distal enhancer upstream of Ihh.

Project description:Mammalian pregnancy depends on the ability of the uterus to support embryo implantation. Previous studies reveal the Sox17 gene as a downstream target of the Pgr-Gata2-dependent transcription network that directs genomic actions in the uterine endometrium receptive for embryo implantation. Here, we report that ablating Sox17 in the uterine epithelium impairs leukemia inhibitory factor (LIF) and Indian hedgehog homolog (IHH) signaling, leading to failure of embryo implantation. In vivo deletion of the SOX17-binding region 19 kb upstream of the Ihh locus by CRISPR-Cas technology reduces Ihh expression specifically in the uterus and alters proper endometrial epithelial-stromal interactions, thereby impairing pregnancy. This SOX17-binding interval is also bound by GATA2, FOXA2, and PGR. This cluster of transcription factor binding is common in 737 uterine genes and may represent a key regulatory element essential for uterine epithelial gene expression.

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SOX17 regulates uterine epithelial-stromal crosstalk acting via a distal enhancer upstream of Ihh

Project description:This SuperSeries is composed of the SubSeries listed below.

2018-08-09 | GSE118328 | GEO

Temporal RNA-seq expression profiling of Sox17-medaited XEN conversion of ESCs

Project description:The transcription factor Sox17 is expressed in early primitive endoderm-fated cells of the mouse embryo and in embryo-derived extraembryonic endoderm (ExEn) stem (XEN) cells. We have shown that overexpression of Sox17 in mouse embryonic stem cells (ESCs) drives cell fate to a committed XEN-like cell state (Sox17-XEN cells). When placed back into the embryo, Sox17-XEN cells contribute exclusively to the ExEn. Transient Sox17 expression is sufficient to drive this fate change during which time cells transit through distinct intermediate states prior to the generation of functional XEN-like cells. We identified dynamic regulatory networks driving Sox17-mediated XEN conversion by analyzing a dynamic regulatory map of gene expression bifurcation points throughout conversion, created using RNA-seq time series data. We found that Sox17 orchestrates this conversion process by acting in autoregulatory and feed-forward network motifs, regulating dynamic gene regulatory networks (GRNs) directing cell fate. We have shown that Sox17-mediated XEN conversion provides a powerful tool for understanding the regulation of cell fate changes and for the elucidation of GRNs regulating lineage decisions in the mouse embryo. Total RNA was extracted during a time course of Sox17 overexpression in mouse ESCs at 7 time points as well as from wild-type ESCs and wild-type XEN cells.

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Transcriptomes comparisons of Dhh KO, Ihh KO and Dhh/Ihh DKO ovaries

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Transcriptomes comparisons of Dhh KO, Ihh KO and Dhh/Ihh DKO ovaries

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