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The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells I

ABSTRACT: The naive embryonic stem cells (nESCs) display unique characteristics mirroring naive pluripotency in vivo, but the molecular mechanisms underlying the self-renewal of nESCs remain incompletely understood. Here we analyzed stranded transcriptomes in mouse nESCs and epiblast-like cells (EpiLCs), and identified 135 long non-coding RNAs (lncRNAs) preferentially expressed in nESCs. We further investigated the functions of Lncenc1, a highly abundant lncRNA in mouse nESCs. Knockdown or knockout of Lncenc1 in mouse nESCs leads to significantly decreased expression of core pluripotency genes and significant reduction of colony formation capability. Furthermore, depletion of Lncenc1 down-regulates the glycolysis pathway, as indicated by significant decreases of glycolysis genes expression, glucose consumption, lactate production and Seahorse data. Mechanically, Lncenc1 associates with RNA-binding proteins PTBP1 and HNRNPK functionally. Together, we demonstrate that Lncenc1 regulates the glycolysis in mouse nESCs, suggesting novel functions of lncRNAs in linking energy metabolism and pluripotent stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE116458 | GEO | 2018/08/01

REPOSITORIES: GEO

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The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells II

Project description:The naive embryonic stem cells (nESCs) display unique characteristics mirroring naive pluripotency in vivo, but the molecular mechanisms underlying the self-renewal of nESCs remain incompletely understood. Here we analyzed stranded transcriptomes in mouse nESCs and epiblast-like cells (EpiLCs), and identified 135 long non-coding RNAs (lncRNAs) preferentially expressed in nESCs. We further investigated the functions of Lncenc1, a highly abundant lncRNA in mouse nESCs. Knockdown or knockout of Lncenc1 in mouse nESCs leads to significantly decreased expression of core pluripotency genes and significant reduction of colony formation capability. Furthermore, depletion of Lncenc1 down-regulates the glycolysis pathway, as indicated by significant decreases of glycolysis genes expression, glucose consumption, lactate production and Seahorse data. Mechanically, Lncenc1 associates with RNA-binding proteins PTBP1 and HNRNPK functionally. Together, we demonstrate that Lncenc1 regulates the glycolysis in mouse nESCs, suggesting novel functions of lncRNAs in linking energy metabolism and pluripotent stem cells.

2018-08-01 | GSE116462 | GEO

A long non-coding RNA specifically expressed in early embryos programs the metabolic balance in adult mice

Project description:Long non-coding RNAs (lncRNAs) display higher tissue-specificity than mRNAs. In particular, many lncRNAs are specifically expressed in early embryos, but the physiological functions of most of them remain largely unknown. Here, we show that deficiency of Lncenc1, a lncRNA specifically expressed in early embryos, results in an altered glucose and lipid balance in adult mice. Newly weaned lncenc1-deficient mice have been shown to display higher fasting blood glucose levels and to prefer to use lipids as a fuel source. When mice were fed a normal chow diet (NCD), in which glucose was the main energy source, glucose intolerance and insulin resistance were observed in adult lncenc1-deficient mice. Under high-fat diet (HFD) conditions, however, lncenc1-deficient mice became healthier and could resist food-induced obesity and metabolic disturbances, including liver steatosis and hypercholesterolmia. Furthermore, PPARγ-regulated lipogenesis in liver was reduced in lncenc1-deficient mice fed an HFD, as shown by transcriptome analyses. Interestingly, lncenc1-deficient mouse embryonic fibroblasts (MEFs) showed impaired glycolysis and lipogenesis, suggesting that the metabolic defects may already exist in embryos. Our study provides the first piece of evidence showing the essential roles of embryo-specific lncRNAs in adult metabolism, verifying the “fetal origin” of adult metabolic disorders.

2022-08-02 | GSE135314 | GEO

The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells

Project description:The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells

| PRJNA479473 | ENA

The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells II

Project description:The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells II

| PRJNA478593 | ENA

The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells I

Project description:The Long Noncoding RNA Lncenc1 Regulates Glycolysis in Naive Mouse ES Cells I

| PRJNA478566 | ENA

NANOG alone induces germ cells in primed epiblast in vitro by activation of enhancers [ChIP-seq]

Project description:Nanog, a core pluripotency factor in the inner cell mass of blastocysts, is also expressed in unipotent primordial germ cells (PGCs) in mice, where its precise role is yet unclear. We investigated this in an in vitro model, in which naive pluripotent embryonic stem (ES) cells cultured in basic fibroblast growth factor (bFGF) and activin A develop as epiblast-like cells (EpiLCs) and gain competence for a PGC-like fate. Consequently, bone morphogenetic protein 4 (BMP4), or ectopic expression of key germline transcription factors Prdm1, Prdm14 and Tfap2c, directly induce PGC-like cells (PGCLCs) in EpiLCs, but not in ES cells. Here we report an unexpected discovery that Nanog alone can induce PGCLCs in EpiLCs, independently of BMP4. We propose that after the dissolution of the naive ES-cell pluripotency network during establishment of EpiLCs, the epigenome is reset for cell fate determination. Indeed, we found genome-wide changes in NANOG-binding patterns between ES cells and EpiLCs, indicating epigenetic resetting of regulatory elements. Accordingly, we show that NANOG can bind and activate enhancers of Prdm1 and Prdm14 in EpiLCs in vitro; BLIMP1 (encoded by Prdm1) then directly induces Tfap2c. Furthermore, while SOX2 and NANOG promote the pluripotent state in ES cells, they show contrasting roles in EpiLCs, as Sox2 specifically represses PGCLC induction by Nanog. This study demonstrates a broadly applicable mechanistic principle for how cells acquire competence for cell fate determination, resulting in the context-dependent roles of key transcription factors during development.

2016-01-11 | GSE71932 | GEO

Activin A in combination with ERK1/2 MAPK pathway inhibition sustains propagation of mouse embryonic stem cells

Project description:The combination of Wnt pathway activation by the GSK3 inhibitor and ERK pathway inhibition by the MEK inhibitor, which is known as 2i is a well-established method to maintain mouse embryonic stem cell (mESC) self-renewal. Here we show that Activin A also has the ability to promote naive pluripotency of mESCs when combined with the MEK inhibitor PD0325901. mESCs were efficiently propagated in a medium containing both Activin A and the MEK inhibitor (PD0325901). mESCs cultured in Activin+PD retained a pluripotency state that expresses high levels of naive pluripotency-related transcription factors and is able to differentiate into three germ layers under appropriate conditions. They also showed naive pluripotency features, including the preferential usage of the Oct4 distal enhancer and the self-renewal response to Wnt pathway activation. Our finding provides another way to maintain the naive pluripotency state and reveals a role of Activin/Nodal/TGF-β signaling in stabilizing self-renewal gene regulatory networks in mESCs. To compare the gene expression patterns of naive and primed pluripotency states and their responses to Wnt and ERK1/2 MAPK pathway, we performed genome-wide gene expression analysis of mESCs and EpiLCs, and those treated with Wnt pathway activator alone or Wnt pathway activator combined with ERK1/2 MAPK pathway inhibitior.

2018-11-02 | GSE74963 | GEO

A Molecular Roadmap of the Phased Progression of Pluripotency

Project description:Pluripotency is highly dynamic and progresses through a continuum of pluripotent stem cell states. The two states that bookend the pluripotency continuum, naïve and primed, are well characterized, but our understanding of the intermediate states and the transitions between them remain incomplete. To address this gap in knowledge, using a previously validated system to induce naive mouse embryonic stem cells (ESCs) to post-implantation pre-grastrulating epiblast-like cells (EpiLCs), we generated comprehensive high-temporal-resolution maps of the proteome, phosphoproteome, transcriptome, and epigenome of ESCs transitioning from naïve to primed pluripotency. Our data provide a comprehensive molecular description of the phased progression of pluripotency and a foundation for investigating mechanisms that regulate pluripotent state transitions.

2019-04-04 | GSE117896 | GEO

STAT3-dependent long non-coding RNA Lncenc1 contributes to ES cells pluripotency

Project description:The self-renewal of Embryonic Stem Cells (ESCs) relies on a complex interplay of pluripotency transcription factors and their targets. LIF-activated STAT3 is a key player in regulating stemness by a number of mechanisms, including the transcriptional induction of pluripotency factors and the maintenance of a stern–like epigenetic landscape. However, not much is known about how STAT3 may be involved in the regulation of stem-cell specific non coding RNAs, an important player in the balance between pluripotency and differentiation. Here we identify in mouse ESCs a STAT3-dependent long non coding RNA, Lncenc1, which is required for pluripotency maintenance and mostly localizes to the cytoplasm. Lncenc1 acts as a positive feedback regulator of the LIF-STAT3 axis by competing for the binding of microRNA-128 to the 3’UTR of the core pluripotency factor Klf4 mRNA, enhancing its expression. Our results unveil a novel mechanism for LIF-STAT3-mediated pluripotency.

2023-09-27 | GSE221670 | GEO

Open chromatin profiling on ESC transition to day1- and day2-epiblast-like stem cells

Project description:Identification of open chromatin profiles at ESC, d1EpiLC and d2EpiLC. The accessible chromatin landscape of naive ESCs (Rex1GFPd2 mouse embryonic stem cell line; parental line; E14Tg2a) and their transition to EpiLCs over a two day period was determined using ATAC-seq.

2019-05-11 | E-MTAB-7207 | biostudies-arrayexpress

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