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Single cell RNA-sequencing (scRNA-seq) of ISL1 knockout (KO) or knockdown and NKX2.5 KO compared to WT in cardiac progenitors (CPs) scRNA-seq of ISL1 KO compared to WT in motor neuron progenitors (MNPs)

ABSTRACT: Single cell RNA-sequencing (scRNA-seq) of ISL1 knockout (KO) or knockdown and NKX2.5 KO compared to WT in cardiac progenitors (CPs) scRNA-seq of ISL1 KO compared to WT in motor neuron progenitors (MNPs)

PROVIDER: PRJNA925840 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23152655_1.fastq.gz	Fastqsanger.gz
	SRR23152655_2.fastq.gz	Fastqsanger.gz
	SRR23152656_1.fastq.gz	Fastqsanger.gz
	SRR23152656_2.fastq.gz	Fastqsanger.gz
	SRR23152657_1.fastq.gz	Fastqsanger.gz

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Single cell RNA-sequencing (scRNA-seq) of ISL1 knockout (KO) or knockdown and NKX2.5 KO compared to WT in cardiac progenitors (CPs); scRNA-seq of ISL1 KO compared to WT in motor neuron progenitors (MNPs)

Project description:Previous evidence suggested ISL1 plays unique transcriptional roles between vastly different cell types in developing humans. Single cell RNA-sequencing (scRNA-seq) of in vitro progenitor cells detailed ISL1's cell-type-specific roles in human cardiac progenitors (CPs) and motor neuron progenitors (MNPs). In addition, scRNA-seq confirmed ISL1 and NKX2.5 likely regulate common transcriptional pathways.

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Prospective isolation of ISL1+ cardiac progenitors from human ESCs for myocardial infarction therapy

Project description:The LIM-homeodomain transcription factor ISL1 marks multipotent cardiac progenitors that give rise to cardiac muscle, endothelium, and smooth muscle cells. ISL1+ progenitors can be derived from human pluripotent stem cells, but the inability to efficiently isolate pure populations has limited their characterization. Using a genetic selection strategy, we were able to highly enrich ISL1+ cells derived from human embryonic stem cells. Comparative quantitative proteomic analysis of enriched ISL1+ cells identified ALCAM (CD166) as a surface marker that enabled the isolation of ISL1+ progenitor cells. ALCAM+/ISL1+ progenitors are multipotent and differentiate into cardiomyocytes, endothelial cells, and smooth muscle cells. Transplantation of ALCAM+ progenitors enhances tissue recovery, restores cardiac function and improves angiogenesis through activation of AKT-MAPK signaling in a rat model of myocardial infarction, based on cardiac MRI and histology. Our study establishes a new efficient method for scalable purification of human ISL1+ cardiac precursor cells for therapeutic applications.

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Rathke’s Cleft-Like Cysts Arise From Isl1 Deletion in Murine Pituitary Progenitors

Project description:The transcription factor ISL1 is expressed in pituitary gland stem cells and the thyrotrope and gonadotrope lineages. Pituitary-specific Isl1 deletion causes hypopituitarism with increased stem cell apoptosis, reduced differentiation of thyrotropes and gonadotropes, and reduced body size. Conditional Isl1 deletion causes development of multiple Rathke’s cleft-like cysts, with 100% penetrance. Foxa1 and Foxj1 are abnormally expressed in the pituitary gland and associated with a ciliogenic gene expression program in the cysts. We confirmed expression of FOXA1, FOXJ1 and stem cell markers in human Rathke's cleft cyst tissue, but not craniopharyngiomas, which suggests these transcription factors are useful, pathological markers for diagnosis of Rathke's cleft cysts. These studies support a model whereby expression of ISL1 in pituitary progenitors drives differentiation into thyrotropes and gonadotropes, and without it, activation of FOXA1 and FOXJ1 permits development of an oral epithelial cell fate with mucinous cysts. This pituitary-specific Isl1 mouse knockout sheds light on the etiology of Rathke's cleft cysts and the role of ISL1 in normal pituitary development.

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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.

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ISL1

Project description:ISL1

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scRNA-seq data from GLI3 KO in brain organoids

Project description:To study the effect of GLI3 knockout in brain organoids, we collected scRNA-seq data from 45 day old brain organoids with GLI3 KO

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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.

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Project description:ISL1-binding site

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