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Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (ChIP-seq)

ABSTRACT: Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (ChIP-seq)

PROVIDER: PRJNA542326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9040730.fastq.gz	Fastqsanger.gz
	SRR9040740.fastq.gz	Fastqsanger.gz
	SRR9040750.fastq.gz	Fastqsanger.gz
	SRR9040760.fastq.gz	Fastqsanger.gz
	SRR9040770.fastq.gz	Fastqsanger.gz

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Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2

Project description:Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2

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Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (RNA-seq)

Project description:Developmental cell fate specification is a unidirectional process that can be reverted in response to injury or experimental reprogramming. Whether differentiation and de-differentiation trajectories intersect mechanistically is unclear. Here, we performed comparative screening in lineage-related mouse naïve embryonic stem cells (ESCs) and primed epiblast stem cells (EpiSCs), and identified the constitutively expressed zinc finger transcription factor (TF) Zfp281 as a bi-directional regulator of cell state interconversion. We showed that subtle chromatin occupancy changes in differentiated cells translate into binding and activation of the histone H3 lysine 9 (H3K9) methyltransferase Ehmt1 and the zinc finger TF Zic2 at enhancers and promoters. Genetic gain and loss of function experiments confirmed a critical role of Ehmt1 and Zic2 downstream of Zfp281 both in driving exit from the ESC state, and in restricting EpiSC reprogramming. Our study reveals that cell type-invariant chromatin association of Zfp281 provides an interaction platform for remodeling the cis-regulatory network underlying cellular plasticity.

2019-10-14 | GSE131015 | GEO

Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (ChIP-seq)

2019-10-14 | GSE131014 | GEO

Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (RNA-seq)

Project description:Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2 (RNA-seq)

| PRJNA542328 | ENA

Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2.

Project description:Developmental cell fate specification is a unidirectional process that can be reverted in response to injury or experimental reprogramming. Whether differentiation and de-differentiation trajectories intersect mechanistically is unclear. Here, we performed comparative screening in lineage-related mouse naïve embryonic stem cells (ESCs) and primed epiblast stem cells (EpiSCs), and identified the constitutively expressed zinc finger transcription factor (TF) Zfp281 as a bidirectional regulator of cell state interconversion. We showed that subtle chromatin binding changes in differentiated cells translate into activation of the histone H3 lysine 9 (H3K9) methyltransferase Ehmt1 and stabilization of the zinc finger TF Zic2 at enhancers and promoters. Genetic gain-of-function and loss-of-function experiments confirmed a critical role of Ehmt1 and Zic2 downstream of Zfp281 both in driving exit from the ESC state and in restricting reprogramming of EpiSCs. Our study reveals that cell type-invariant chromatin association of Zfp281 provides an interaction platform for remodeling the cis-regulatory network underlying cellular plasticity.

| S-EPMC6960450 | biostudies-literature

Zfp281 orchestrates interconversion of pluripotent states by engaging Ehmt1 and Zic2

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-10-14 | GSE131017 | GEO

Autophagy engaging and non-engaging hematopoietic stem cells

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Zic2, an enhancer-binding factor required for embryonic stem cell specification

Project description:The Zinc finger protein of the cerebellum 2 (Zic2) is one of the vertebrate homologs of the Drosophila pair-rule gene odd-paired (opa). Our molecular and biochemical studies have demonstrated that Zic2 to preferentially bind to transcriptional enhancers and functions as a cofactor that interacts with the NuRD complex in ES cells. Detailed genome-wide studies demonstrate that Zic2 function with Mbd3/NuRD in regulating the chromatin state and transcriptional output of genes linked to differentiation. Zic2 is dispensable for the selfrenewal of ES cells but is required for proper differentiation, similar to what has been previously reported for Mbd3/NuRD. Our study identifies Zic2 as a key factor in the execution of the pluripotency program with Mbd3/NuRD in ES cells. ChIP-seq of Zic2, Chd4, Mbd3 and Zic3 in mES cells. ChIP-seq of H3K27me3, H3K27ac, H3K4me3, H3K4me1 and PolII in mES cells after Zic2 shRNA and non-targeting shRNA. RNA-seq of mES cells after Zic2, Zic3, Mbd3 and Mta2 shRNA and non-targeting shRNA.

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Zfp281 Functions as a Transcriptional Repressor for Pluripotency of Mouse Embryonic Stem Cells

Project description:Zfp281 is a partner protein of Nanog. To identify potential target genes of Zfp281, we generated Zfp281 null ESCs using gene targeting, and compared transcriptomic changes between multiple lines of wildtype, heterozygous and null ESCs. Total 8 ESC lines: 3 wildtype lines, 2 heterozygous lines, and 3 null lines.

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Post-natal supply of GLP/Ehmt1 reverses Histone H3K9 dimethylation in cortical neuron isolated from adult Ehmt1∆/+ mice brain

Project description:EHMT1 haploinsufficiency causes Kleefstra syndrome (KS), a complex disorder of developmental delay and intellectual disability. EHMT1 encodes a lysine methyltransferase GLP and regulates histone H3 lysine 9 dimethylation (H3K9me2). Ehmt1 heterozygous mutant (Ehmt1∆/+) mice show KS-like abnormal behavioral phenotypes. Here, we examined the reversibility of decreased H3K9me2 by postnatal supply of GLP in post-mitotic neuron of Ehmt1∆/+ mice brain. For this purpose, we generated the mice harboring inducible Ehmt1 cDNA with CamKII-creER (Ehmt1 iTG-neuron mice) in Ehmt1∆/+ background. These mice expressed exogenous Ehmt1 in post-mitotic neuron upon Tamoxifen treatment. Using these mice, we sorted out NeuN+ cells from cortical region and performed Histone H3 K9-dimethyation ChIP analysis. Here we showed that Ehmt1 haploinsufficiency induces global reduction of euchromatic H3K9me2 especially in the euchromatic region of brain and that postnatal supply of GLP can reverse the diminished H3K9me2 phenotype, even in a postmitotic situation.

2021-06-09 | GSE162327 | GEO

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