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Analysis of transposable element expression in mouse ESCs with and without Ncor1, and a time course RNA-seq of mouse ESC differentiation to EpiLCs

ABSTRACT: Analysis of transposable element expression in mouse ESCs with and without Ncor1, and a time course RNA-seq of mouse ESC differentiation to EpiLCs

PROVIDER: PRJNA566099 | ENA |

REPOSITORIES: ENA

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Analysis of transposable element expression in mouse ESCs with and without Ncor1, and a time course RNA-seq of mouse ESC differentiation to EpiLCs

Project description:Mouse embryonic stem cells (ESCs) were differentiated to Epiblast-like cells (EpiLCs) according to the protocol in Hayashi et al., 2011. Samples were taken at 0, 12, 24, 36 and 48 hours. Wildtype and Ncor2 knockout ESCs were also sequenced to measure gene expression.

2020-07-22 | GSE137627 | GEO

Single-cell transcriptome profiling during the in vitro differentiation of mouse ESCs (mESCs) into epiblast-like cells (EpiLCs).

Project description:We performed single-cell RNA sequencing (RNA-seq) during the in vitro transition of mouse ESCs (mESCs) from a naïve pluripotent state into epiblast-like cells (EpiLCs), a primed pluripotent state. We derived pseudotime expression trajectories to investigate transcript dynamics of key metabolic regulators, with the aim to identify metabolic pathways that potentially impact on early embryonic cell state transitions.

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Transcriptomes of mouse PGCLCs isolated from 6-day culture embryoid bodies were compared with transcriptomes of their precur cells (ESCs, iPSCs, and EpiLCs) and E12.5 in vivo mouse PGCs

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Transcriptomes of mouse PGCLCs isolated from 6-day culture embryoid bodies were compared with transcriptomes of their precur cells (ESCs, iPSCs, and EpiLCs) and E12.5 in vivo mouse PGCs

Project description:Transcriptomes of mouse E12.5 primordial germ cells (PGCs), primordial germ cell-like cells (PGCLCs) isolated from 6-day culture embryoid bodies, and the precursor pluripotent stem cells [embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs)] and epiblast-like cells (EpiLCs) Total RNA was isolated from FACS-enriched, SSEA1+/CD61+ double-positive PGCs and PGCLCs. RNA was also isolated from ESC, iPSC, and EpiLC cultured without enrichment. Transcriptomes were determined using Affymetrix microarray.

2016-08-22 | E-GEOD-80983 | biostudies-arrayexpress

The Fgf/Erf/NCoR1/2 repressive axis controls trophoblast cell fate

Project description:Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with components of the Nuclear Receptor Corepressor Complex 1 and 2 (NCoR1 and NCoR2). Upon attenuation of Fgf signalling, unphosphorylated, nuclear Erf recruits the NCoR1/2 complex to key trophoblast genes, brings about their transcriptional silencing and facilitates differentiation and placental development.

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DNA methylation and hydroxymethylation profiles were compared between mouse PGCLCs isolated from 6-day culture embryoid bodies, their precursor cells (ESCs, iPSCs, and EpiLCs), and E12.5 in vivo mouse PGCs.

Project description:DNA methylation and hydroxymethylation in the genomes of mouse E12.5 primordial germ cells (PGCs), primordial germ cell-like cells (PGCLCs) isolated from 6-day culture embryoid bodies, and the precursor pluripotent stem cells [embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs)] and epiblast-like cells (EpiLCs)

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NCoR1, SMRT, Polymerase II and input ChIP-Seq

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NCoR1 and SMRT play unique roles in thyroid hormone signaling in the liver

Project description:NCoR1 (Nuclear receptor Co-Repressor) and SMRT (Silencing Mediator of Retinoid and Thyroid hormone receptor) are well-recognized coregulators of nuclear receptor (NR) action. However, their unique roles in the regulation of thyroid hormone (TH) signaling in specific cell types have not been determined. To accomplish this we generated a mouse model that lacked function of either NCoR1 or SMRT or both in the liver only. Despite both corepressors being present in the liver, SMRT had no ability to regulate TH signaling when deleted in either euthyroid or hypothyroid animals. In contrast, disruption of NCoR1 action confirmed that it is the principal mediator of TH sensitivity in vivo. While SMRT played little role in TH signaling alone, when disrupted in combination with NCoR1 it greatly accentuated the activation of hepatic lipogenesis regulated by NCoR1. Thus, corepressor specificity exists in vivo and NCoR1 is the principal regulator of TH action in the liver. However, both NCoR1 and SMRT collaborate to control hepatic lipogenesis and lipid storage, which likely reflects their cooperative activity in regulating the action of multiple NRs including the thyroid hormone receptor (TR). RNA was extracted from livers from 3 individual mice for each group (Double-floxed, Liver specific-SMRT knock out, and Liver specific-double knock out); all were euthyroid, female mice

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Project description:Placental development relies on coordinated cell fate decisions governed by signalling inputs. However, little is known about how signalling cues are transformed into repressive lineage-specific transcriptional signatures. Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with the Nuclear Receptor Corepressor Complex 1 and 2 (NCoR1/2) and recruits it to key trophoblast genes. Genetic ablation of Erf or Tbl1x (a component of the NCoR1/2 complex) abrogates the Erf/NCoR1/2 interaction. This leads to mis-expression of Erf/NCor1/2 target genes resulting in a TSC differentiation defect. Mechanistically, Erf regulates expression of these genes by recruiting the NCoR1/2 complex to their enhancers and modulation of H3K27ac. Our findings uncover how the Fgf/Erf/NCoR1/2 repressive axis governs cell fate and placental development, providing a new paradigm for Fgf-mediated transcriptional control.

2023-04-26 | GSE199024 | GEO

Gene expression analysis of Ncor1 muscle-specific knockout and PGC-1alpha muscle-specific transgenic skeletal muscle

Project description:In the present study we have studied the mechanistic and functional aspects of NCoR1 function in mouse skeletal muscle. NCoR1 muscle-specific knockout mice exhibited an increased oxidative metabolism. Global gene expression analysis revealed a high overlap between the effects of NCoR1 deletion and peroxisome proliferator-activated receptor (PPAR) gamma coactivator 1alpha (PGC-1alpha) overexpression on oxidative metabolism in skeletal muscle. The repressive effect of NCoR1 on oxidative phosphorylation gene expression specifically antagonizes PGC-1alpha-mediated coactivation of ERRalpha. We therefore delineated the molecular mechanism by which a transcriptional network controlled by corepressor and coactivator proteins determines the metabolic properties of skeletal muscle, thus representing a potential therapeutic target for metabolic diseases. Gene expression of a total of 20 gastrocnemius samples from control (CON, n = 5), NCoR1 muscle-specific knockout (NCoR1 MKO, n = 5), wild type (WT, n = 5) and PGC-1alpha muscle-specific transgenic (PGC-1alpha mTg, n = 5) adult male mice was analyzed using GeneChipÂ® Gene 1.0 ST Array System (Affymetrix). NCoR1 MKO and PGC-1alpha mTg samples were compared to CON and WT samples, respectively.

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