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Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Pancreas RNA-seq]

ABSTRACT: Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Pancreas RNA-seq]

PROVIDER: PRJNA748594 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15206351_1.fastq.gz	Fastqsanger.gz
	SRR15206351_2.fastq.gz	Fastqsanger.gz
	SRR15206352_1.fastq.gz	Fastqsanger.gz
	SRR15206352_2.fastq.gz	Fastqsanger.gz
	SRR15206353_1.fastq.gz	Fastqsanger.gz

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Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Pancreas RNA-seq]

Project description:Tbx3 regulates liver development in the mouse, but it's role in human liver development is unclear. We generated TBX3 knockout pluripotent stem cell lines and found that liver differentiation is also impaired in humans. Interestingly we noted expression of pancreas-specific genes during the liver differentiation in the TBX3 knockout line.To further investigate this phenomenon, we performed RNA-seq on cells from two stages of the pancreatic differentation. These studies demonstrated that the loss of TBX3 enhances pancreatic-gene signature, implicating TBX3 as a regulator of fate decisions.

2021-10-14 | GSE180525 | GEO

Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast ATAC-seq]

Project description:Tbx3 regulates liver development in the mouse, but it's role in human liver development is unclear. We generated TBX3 knockout pluripotent stem cell lines and found that liver differentiation is also impaired in humans. Interestingly we noted expression of pancreas-specific genes during the liver differentiation in the TBX3 knockout line. To further investigate this phenomenon, we performed ATAC-seq on cells at the hepatoblast stage of the liver differentiation. These studies demonstrated that the loss of TBX3 enhances pancreatic-gene signature, implicating TBX3 as a regulator of fate decisions.

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Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast RNA-seq]

Project description:Tbx3 regulates liver development in the mouse, but it's role in human liver development is unclear. We generated TBX3 knockout pluripotent stem cell lines and found that liver differentiation is also impaired in humans. Interestingly we noted expression of pancreas-specific genes during the liver differentiation in the TBX3 knockout line. To further investigate this phenomenon, we performed RNA-seq on cells at the hepatoblast stage of the liver differentiation. These studies demonstrated that the loss of TBX3 enhances pancreatic-gene signature, implicating TBX3 as a regulator of fate decisions.

2021-10-14 | GSE180526 | GEO

Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells

Project description:Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells

| PRJNA748588 | ENA

Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast RNA-seq]

Project description:Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast RNA-seq]

| PRJNA748592 | ENA

Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast ATAC-seq]

Project description:Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells [Hepatoblast ATAC-seq]

| PRJNA748593 | ENA

Loss of TBX3 enhances pancreatic progenitor generation from human pluripotent stem cells.

Project description:Tbx3 has been identified as a regulator of liver development in the mouse, but its function in human liver development remains unknown. TBX3 mutant human pluripotent stem cell (PSC) lines were generated using CRISPR/Cas9 genome editing. TBX3 loss led to impaired liver differentiation and an upregulation of pancreatic gene expression, including PDX1, during a hepatocyte differentiation protocol. Other pancreatic genes, including NEUROG3 and NKX2.2, displayed more open chromatin in the TBX3 mutant hepatoblasts. Using a pancreatic differentiation protocol, cells lacking TBX3 generated more pancreatic progenitors and had an enhanced pancreatic gene expression signature at the expense of hepatic gene expression. These data highlight a potential role of TBX3 in regulating hepatic and pancreatic domains during foregut patterning, with implications for enhancing the generation of pancreatic progenitors from PSCs.

| S-EPMC8580886 | biostudies-literature

Tbx3 controls Dppa3 levels to regulate exit from pluripotency towards mesodermal lineage

Project description:Tbx3, a member of the T-box family, plays important roles in development, stem cells, nuclear reprogramming and cancer. Loss of Tbx3 induces differentiation in mouse embryonic stem cells (mESCs). However, we show that mESCs exist in an alternate stable pluripotent state in the absence of Tbx3. In-depth transcriptome analysis of this mESC state reveals Dppa3 as a direct downstream target of Tbx3. Also Tbx3 facilitates the cell fate transition from pluripotent cells to mesoderm progenitors by directly repressing Wnt pathway members required for differentiation. Wnt signaling regulates differentiation of mESCs into mesoderm progenitors and helps maintain a naïve pluripotent state. We show that Tbx3, a downstream target of Wnt signaling, fine-tunes these divergent roles of Wnt signaling in mESCs. In conclusion, we identify a signaling-TF axis that controls the exit of mESCs from a self-renewing pluripotent state towards mesoderm differentiation. ChIPSeq and RNASeq (population and single cell) was performed on the indicated cell lines. Replicates are indicated as needed. The mm9 genome assembly was used. For single cell mRNA-Seq preparation, SSEA1+DAPI- mESCs were sorted and collected.

2015-07-21 | E-GEOD-60066 | biostudies-arrayexpress

Tbx3 controls Dppa3 levels to regulate exit from pluripotency towards mesodermal lineage

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Tbx3 improves the germ-line competency of induced pluripotent stem cells

Project description:Induced pluripotent stem (iPS) cells can be obtained through the introduction of defined factors into somatic cells. The combination of Oct4, Sox2 and Klf4 (OSK) constitutes the minimal requirement for generating iPS cells from mouse embryonic fibroblasts (MEFs). These cells are thought to resemble embryonic stem cells (ESCs) based on global gene expression analyses; but, few studies have tested their ability and efficiency in contributing to chimerism, colonization of germ tissues, and most importantly, germ-line transmission and life-birth from iPS cells produced with tetraploid complementation. Through the genomic analyses of ESC genes that have roles in pluripotency and fusion-mediated somatic cell reprogramming, we identified Tbx3 as a transcription factor that significantly improves the quality of iPS cells. Induced-PS cells generated with OSK + Tbx3 (OSKT) are superior in both germ cell contribution to the gonads and germ-line transmission frequency. However, global gene expression profiling could not distinguish between OSK and OSKT iPS cells. Genome-wide ChIP-sequencing analysis of Tbx3 binding sites in ESCs suggests that Tbx3 regulates pluripotency-associated and reprogramming factors, in addition to sharing many common downstream regulatory targets with Oct4, Sox2, Nanog and Smad1. This study underscores the intrinsic qualitative differences between iPS cells generated by different methods and highlights the need to rigorously characterize iPS cells beyond in vitro studies.

2009-11-25 | GSE19164 | GEO

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