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Kap1 ChIP-seq Analysis of Wild Type(WT) and Dcaf11 overexpresion(OE) ESCs

ABSTRACT: Kap1 ChIP-seq Analysis of Wild Type(WT) and Dcaf11 overexpresion(OE) ESCs

PROVIDER: PRJNA681174 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13156259_1.fastq.gz	Fastqsanger.gz
	SRR13156259_2.fastq.gz	Fastqsanger.gz
	SRR13156260_1.fastq.gz	Fastqsanger.gz
	SRR13156260_2.fastq.gz	Fastqsanger.gz
	SRR13156261_1.fastq.gz	Fastqsanger.gz

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Kap1 ChIP-seq Analysis of Wild Type(WT) and Dcaf11 overexpresion(OE) ESCs

Project description:ESC Kap1 profiles of WT and Dcaf11 OE were generated by deep sequencing, using Illumina GAIIx.

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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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ULI-NChIP-seq Analysis of Wild Type(WT) and Dcaf11 overexpresion(OE) ESCs [ChIP-seq]

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

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

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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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Project description:Chromatin remodeling is fundamental for B cell differentiation. Here, we explored the role in this process of KAP1, the cofactor of KRAB-ZFP transcriptional repressors. B lymphoid-specific Kap1 knockout mice displayed reduced numbers of mature B cells, lower steady-state levels of antibodies and accelerated rates of decay of neutralizing antibodies following viral immunization. Transcriptome analyses of Kap1-deleted B splenocytes revealed an upregulation of PTEN, the enzymatic counter-actor of PIK3 signaling, and of genes encoding DNA damage response factors, cell-cycle regulators and chemokine receptors. ChIP/seq studies established that KAP1 bound at or close to a number of these genes, and controlled chromatin status at their promoters. Genome-wide, KAP1-binding sites avoided active B cell-specific enhancers and were enriched in repressive histone marks, further supporting a role for this molecule in gene silencing in vivo. Likely responsible for tethering KAP1 to at least some of these targets, a discrete subset of KRAB-ZFPs is enriched in B lymphocytes. This work thus reveals the role of KRAB/KAP1-mediated epigenetic regulation in B cell development and homeostasis. Follicular (FO) and Transcriptional 2 Follicular Progenitor (T2-FP) B cells were sorted out from 3 CD19-Cre/Kap1flox (KAP1 KO in the B lineage) mice and 3 wt/Kap1flox littermate controls

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