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Function of deubiquitinase USP21 in mouse embryonic stem cell [RNA-Seq]

ABSTRACT: Ubiquitination-mediated protein degradation of key transcriptional factors is important to the self-renewal of embryonic stem (ES) cells. However, little is known about the deubiquitination in ES self-renewal and differentiation. Here, we report that deubiquitinase USP21 is an important positive regulator to keep ES cells under undifferentiation stasus by deubiquitination and stabilization of Nanog, a key transcriptional factor of ES cells. Loss of USP21 led to ES cells differentiation and defect in reprogramming.

ORGANISM(S): Mus musculus

PROVIDER: GSE69987 | GEO | 2016/10/05

SECONDARY ACCESSION(S): PRJNA287352

REPOSITORIES: GEO

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Function of deubiquitinase USP21 in mouse embryonic stem cell [ChIP-Seq]

Project description:Nanog is a master pluripotency factor of embryonic stem cells (ESCs). Stable expression of Nanog is required to maintain the stemness of ESCs, although Nanog is a short-lived protein and quickly degraded by the ubiquitin-dependent proteasome system (UPS). Here, we report that the deubiquitinase USP21 interacts with, deubiquitinates and stabilizes Nanog and therefore maintains the protein level of Nanog in mouse-ESCs (mESCs). Loss of USP21 results in Nanog destruction, mESCs differentiation and reduced the somatic cell reprogramming efficiency. USP21 is a transcriptional target of the LIF/STAT3 pathway and is downregulated upon differentiation. Moreover, differentiation cues promote ERK-mediated phosphorylation and dissociation of USP21 from Nanog, thus leading to Nanog degradation. Additionally, USP21 is recruited to gene promoters by Nanog to deubiquitinate histone H2A at K119 and thus facilitates Nanog-mediated gene expression. Together, our findings provide a regulatory mechanism by which extrinsic signals regulate mESC fate via deubiquitinating Nanog.

2016-10-05 | GSE79890 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of FOXP3-YFP-Cre and FOXP3-YFP-Cre/USP21-floxp/floxp Treg Cells Transcriptomes

Project description:Regulatory T (Treg) cells harbor immune suppressive capacity and are crucial for the maintenance of peripheral tolerance. Treg cells are considered to be heterogenic, where compromised FOXP3 expression results in the generation of exTreg cells. Here we report that the E3 deubiquitinase USP21 prevents the depletion of FOXP3 protein and restricts tissue-resident exTreg cell generation. Mice lacking USP21 in Treg cells display immune disorders characterized by spontaneous T cell activation and excessive T helper type 1 (Th1) skewing. USP21 stabilizes FOXP3 protein by mediating its deubiquitination and therefore helps to maintain the expression of Treg signature genes. Moreover, at inflamed loci, tissue-resident USP21-deficient Treg cells display a Th1-like effector phenotype. Therefore, we demonstrate how USP21 controls the identity of tissue-resident Treg cells by preventing FOXP3 loss.

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Function of deubiquitinase USP21 in mouse embryonic stem cell

Project description:Function of deubiquitinase USP21 in mouse embryonic stem cell

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Project description:USP21 belongs to ubiquitin specific protease (USP) family. To dissect the molecular mechanisms that regulated by USP21 overexpression in PDAC cells, we conducted RNA-seq analysis of iKPC PDAC cells overexpressing wild-type USP21 (WT-USP21) and enzyme dead USP21 (ED-USP21).

2019-09-04 | GSE134686 | GEO

Effect of USP21 deficiency on transcriptomes in skeletal muscle of mice

Project description:Skeletal muscle is the pivotal organ for energy homeostasis, but the regulatory mechanisms are largely unknown. Here, we report that ubiquitin specific protease 21 (USP21) is a regulator of skeletal muscle physiology. To elucidate features important for USP21, we performed RNA-sequencing analysis using the muscle tissue of muscle-specific USP21 knockout (USP21-MKO) mice or wild-type littermates with floxed genotype, screened and analyzed the differentially expressed genes. Transcriptomics assay enabled us to discover major signaling nodes persistently activated by USP21 ablation in close association with the genes linked to fuel oxidation. Consequently, USP21 ablation altered gross metabolic phenotypes.

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RNAseq data comparing GFP, wildtype USP21 and enzyme-dead USP21 overexpressing iKPC PDAC cells with KRAS* expression (on dox) and KRAS* extinction (off dox)

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The deubiquitinase Usp9x regulates PRC2-mediated chromatin reprogramming during mouse development

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2021-01-25 | GSE146800 | GEO

Changes in Treg gene expression upon deletion of Usp22 and Usp21

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RNAseq data comparing iKPC cells overexpressing WT-USP21 and ED-USP21

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Regulation of B lymphocyte development by histone H2A deubiquitinase BAP1 (Bap1KO_RNA-Seq)

Project description:BAP1 is a deubiquitinase (DUB) of the Ubiquitin C-terminal Hydrolase (UCH) family that regulates gene expression and other cellular processes, via deubiquitination of histone H2AK119ub and other substrates. BAP1 is an important tumour suppressor in human, expressed and functional across many cell-types and tissues, including those of the immune system. B lymphocytes are the mediators of humoral immune response, however the role of BAP1 in B cell development and physiology remains poorly understood. Here we characterize a mouse line with a selective deletion of BAP1 within the B cell lineage (Bap1fl/fl mb1-Cre) and establish a cell intrinsic role of BAP1 in the regulation of B cell development. We demonstrate a depletion of large pre-B cells, transitional B cells, and mature B cells in Bap1fl/fl mb1-Cre mice. We characterize broad transcriptional changes in BAP1-deficient pre-B cells, map BAP1 binding across the genome, and analyze the effects of BAP1-loss on histone H2AK119ub levels and distribution. Overall, our work establishes a cell intrinsic role of BAP1 in B lymphocyte development, and suggests its contribution to the regulation of the transcriptional programs of cell cycle progression, via the deubiquitination of histone H2AK119ub.

2021-03-29 | GSE162084 | GEO

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