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Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

ABSTRACT: Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

PROVIDER: PRJNA1036587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26701040_1.fastq.gz	Fastqsanger.gz
	SRR26701040_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

| PRJNA1036585 | ENA

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

Project description:Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

| PRJNA1036588 | ENA

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [RNA-Seq]

Project description:The transcription factor Isl1 is expressed in the progenitors of the Ex-Mes and allantois, however its role in the placentation remains unclear. Our studies showed that deletion of Isl1 causes defects in allantois growth, chorioallantoic fusion and placenta vessel morphogenesis. RNA-seq analyses have revealed that Isl1 regulates the expression of genes important for Ex-Mes multipotency, differentiation and diversification. Isl1 promotes allantoic endothelial but inhibits mesenchymal cell differentiation. Isl1 plays an important role in regulating multiple genetic and epigenetic pathways of vascular morphogenesis. Allantoic signals regulated by Isl1 in turn mediate the inductive interactions between the allantois and chorion critical for chorionic epithelium differentiation, villous formation, and labyrinth angiogenesis. In conclusion, our study provides an integrated insight into the mechanisms underlying placental lineage differentiation, diversification, and vascular formation, highlighting the necessity of Isl1 for early placenta morphogenesis. Our study suggests the potential utility of Isl1 in regenerative medicine application using the stem cells derived from the placenta, umbilical cord and amnionic membrane.

2024-09-13 | GSE247182 | GEO

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation [CUT&Tag]

Project description:To uncover direct targets of ISL1 that could account for its role in allantois, we performed cut tag analysis on wild type allantoic cells using ISL1 antibody at E8.75. Our analyses uncovered 5509 significant binding peaks for ISL1, mainly located at intergenic or intronic regions.

2024-09-13 | GSE247183 | GEO

Isl1 identifies the extraembryonic mesodermal / allantois progenitors and required for placenta morphogenesis and vasculature formation

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

2024-09-13 | GSE247184 | GEO

Isl Identifies the Extraembryonic Mesodermal/Allantois Progenitors and is Required for Placenta Morphogenesis and Vasculature Formation.

Project description:The placenta links feto-maternal circulation for exchanges of nutrients, gases, and metabolic wastes between the fetus and mother, being essential for pregnancy process and maintenance. The allantois and mesodermal components of amnion, chorion, and yolk sac are derived from extraembryonic mesoderm (Ex-Mes), however, the mechanisms contributing to distinct components of the placenta and regulation the interactions between allantois and epithelium during chorioallantoic fusion and labyrinth formation remains unclear. Isl1 is expressed in progenitors of the Ex-Mes and allantois the Isl1 mut mouse line is analyzed to investigate contribution of Isl1+ Ex-Mes / allantoic progenitors to cells of the allantois and placenta. This study shows that Isl1 identifies the Ex-Mes progenitors for endothelial and vascular smooth muscle cells, and most of the mesenchymal cells of the placenta and umbilical cord. Deletion of Isl1 causes defects in allantois growth, chorioallantoic fusion, and placenta vessel morphogenesis. RNA-seq and CUT&Tag analyses revealed that Isl1 promotes allantoic endothelial, inhibits mesenchymal cell differentiation, and allantoic signals regulated by Isl1 mediating the inductive interactions between the allantois and chorion critical for chorionic epithelium differentiation, villous formation, and labyrinth angiogenesis. This study above reveals that Isl1 plays roles in regulating multiple genetic and epigenetic pathways of vascular morphogenesis, provides the insight into the mechanisms for placental formation, highlighting the necessity of Isl1 for placenta formation/pregnant maintenance.

| S-EPMC11348239 | biostudies-literature

Effect of depletion of Isl1 on gene expression at 8.75 days of embryo development

2024-09-13 | GSE245625 | GEO

ISL1

Project description:ISL1

| PRJNA312204 | ENA

Protein Kinase C Establishes the Signaling Boundary Between Mesodermal and Extraembryonic Lineages in Human Embryonic Stem Cell Differentiation

Project description:The interplay among mitogenic signaling pathways is crucial for proper embryogenesis. These pathways collaboratively act through intracellular master regulators to determine specific cell fates. Identifying the master regulators is critical to understanding embryogenesis and to developing new applications of pluripotent stem cells. In this report, we demonstrate protein kinase C (PKC) as an intrinsic master switch between embryonic and extraembryonic cell fates in the differentiation of human pluripotent stem cells (hPSCs). PKCs are essential to inducing the extraembryonic lineage downstream of various mitogenic modulators. PKC-alpha (PKCα) suppresses BMP4-induced mesoderm differentiation, and PKC-delta (PKCδ) is required for extraembryonic trophoblast cell fate. PKC activation overrides mesoderm induction conditions and leads to extraembryonic fate. In contrast, PKC inhibition leads to β-catenin activation, switching cell fate from extraembryonic to mesoderm lineages. This study establishes PKC as a central player directing the segregation of extraembryonic and embryonic lineages. The manipulation of intrinsic PKC activity could greatly enhance cell differentiation under mitogenic regulation in stem cell applications.

2022-03-08 | GSE198006 | GEO

ISL1-binding site

Project description:ISL1-binding site

| PRJNA505254 | ENA