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Klf5 regulates trophoblast stem cell pluripotency as a transcription activator via H3K27ac dependent chromatin accessibility

ABSTRACT: Klf5 regulates trophoblast stem cell pluripotency as a transcription activator via H3K27ac dependent chromatin accessibility

PROVIDER: PRJNA853374 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19878640_1.fastq.gz	Fastqsanger.gz
	SRR19878640_2.fastq.gz	Fastqsanger.gz
	SRR19878641_1.fastq.gz	Fastqsanger.gz
	SRR19878641_2.fastq.gz	Fastqsanger.gz
	SRR19878642_1.fastq.gz	Fastqsanger.gz

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Klf5 regulates trophoblast stem cell pluripotency as a transcription activator via H3K27ac dependent chromatin accessibility

Project description:The effective proliferation and differentiation of Trophoblast Stem Cells (TSCs) is necessary to ensure the normal development of the placenta, which is the key to maintain fetal growth and development during pregnancy. Previous studies have found that knocking out Klf5 affects abnormally trophoderm development, but its regulatory mechanism is unclear. Here we performed klf5 knockdown in TSCs cultured under stem state condition. Klf5-KD triggred obvious differentiation phenotype.

2022-09-27 | GSE207053 | GEO

WT vs Klf5 KO ES

Project description:Homozygous disruption of Bteb2/Klf5, a homolog of Drosophila gap gene Krüppel, led to increased expression of various differentiation marker genes, such as Fgf5, Cdx2, and Brachyury in mouse ES cells without compromising their ability to differentiate into all three germ layers. Upon removal of LIF, Klf5-deficient ES cells showed faster differentiation kinetics than wild-type ES cells. In contrast, overexpression of Klf5 in ES cells suppressed the transcription of differentiation marker genes, and maintained pluripotency in the absence of LIF. In order to search downstream genes of Klf5, we surveyed genes implicated in ES cell proliferation by microarray analysis Keywords: cell type comparison

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A balanced Oct4 protein interaction network is crucial for maintaining pluripotency

Project description:Oct4 is considered a master transcription factor for pluripotent cell self-renewal and embryo development. It primarily collaborates with other transcriptional factors or coregulators to maintain pluripotency. However, it is still unclear how Oct4 interacts with its partners. Here, we show that the Oct4 linker interface mediates competing and balanced Oct4 protein interactions which are crucial for maintaining pluripotency. Linker mutant ESCs maintain the key pluripotency genes expression, but show decreased expression of self-renewal genes and increased expression of differentiation genes which result in impaired ESCs self-renewal and early embryonic lethality. Linker mutation dose not affect Oct4 genomic binding and transactivation potential, but breaks the balanced Oct4 interactome. In mutant ESCs, the interaction between Oct4 and Klf5 was decreased, but interactions between Oct4 and Cbx1, Ctr9, Cdc73 were increased which disrupt the epigenetic state of ESCs. Overexpression of Klf5 or knockdown Cbx1, Cdc73 rescue the cellular phenotype of linker mutant ESCs by rebalancing Oct4 interactome indicating that different partners interact with Oct4 competitively. Thus, by showing how Oct4 interacts with different partners, we provide novel molecular insights to explain how Oct4 contributes to the maintenance of pluripotency.

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Project description:We identified the binding profile of Klf4 and Klf5, which are both transcription facyors involved in the maintenance of pluripotency of ESCs by inhibiting their differentiation either into endoderm or mesoderm respectively. Undifferentiated mouse ESCs were used to identify Klf4 and Klf5 bidning sites

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Project description:We used ChIP-seq to map the binding sites of wild-type and mutant KLF5. In addition, by performing H3K27ac ChIP-seq, we mapped the enhancer regions in cell lines of head and neck squamous cell carcinomas, esophageal carcinomas, and stomach adenocarcinomas.

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Klf5 OE ES

Project description:Klf5 OE ES

| PRJNA1026845 | ENA