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Single cell RNA-seq Analysis of Wild Type(WT), Dcaf11 knockout(KO) and Dcaf11 knockdown(KD) embryos

ABSTRACT: Single cell RNA-seq Analysis of Wild Type(WT), Dcaf11 knockout(KO) and Dcaf11 knockdown(KD) embryos

PROVIDER: PRJNA548909 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9302940_1.fastq.gz	Fastqsanger.gz
	SRR9302940_2.fastq.gz	Fastqsanger.gz
	SRR9302941_1.fastq.gz	Fastqsanger.gz
	SRR9302941_2.fastq.gz	Fastqsanger.gz
	SRR9302932_1.fastq.gz	Fastqsanger.gz

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Single cell RNA-seq Analysis of Wild Type(WT), Dcaf11 knockout(KO) and Dcaf11 knockdown(KD) embryos

Project description:Telomeres play vital roles in ensuring chromosome stability and are thus closely linked with the onset of aging and human disease. Telomeres undergo extensive lengthening during early embryogenesis through the so-called alternative lengthening of telomere (ALT) mechanism. However, the detailed molecular mechanism of telomere resetting in early embryos remains unknown. Here, we showed that Dcaf11 participates in telomere elongation in early embryos and 2-cell-like embryonic stem cells (ESCs) in a telomerase-independent manner. The deletion of Dcaf11 in embryos and ESCs leads to reduced telomere sister-chromatid exchange (T-SCE) and impairs telomere lengthening. Importantly, Dcaf11-deficient mice exhibit gradual telomere erosion with successive generations, and hematopoietic stem cell (HSC) activity is greatly compromised. Mechanistically, DCAF11 reactivates Zscan4 and facilitates the removal of heterochromatic H3K9me3 at telomere/subtelomere regions through targeting TRIM28 for ubiquitination-mediated degradation. Our study therefore demonstrates that the ALT factor Dcaf11 plays important roles in telomere elongation in early embryos and ESCs.

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RNA-seq Analysis of Wild Type(WT) and Dcaf11 overexpression (OE) ESCs

Project description:Telomeres play vital roles in ensuring chromosome stability and are thus closely linked with the onset of aging and human disease. Telomeres undergo extensive lengthening during early embryogenesis. However, the detailed molecular mechanism of telomere resetting in early embryos remains unknown. Here, we show that Dcaf11 (Ddb1- and Cul4-associated factor 11) participates in telomere elongation in early embryos and 2-cell-like embryonic stem cells (ESCs). The deletion of Dcaf11 in embryos and ESCs leads to reduced telomere sister-chromatid exchange (T-SCE) and impairs telomere lengthening. Importantly, Dcaf11-deficient mice exhibit gradual telomere erosion with successive generations, and hematopoietic stem cell (HSC) activity is also greatly compromised. Mechanistically, Dcaf11 targets Kap1 (KRAB-associated protein 1) for ubiquitination-mediated degradation, leading to the activation of Zscan4 downstream enhancer and the removal of heterochromatic H3K9me3 at telomere/subtelomere regions. Our study therefore demonstrates that Dcaf11 plays important roles in telomere elongation in early embryos and ESCs through activating Zscan4.

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Project description:Our study demonstrates that Dcaf11 plays important roles in telomere elongation in early embryos and ESCs through activating Zscan4.

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