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Mouse_embryoid Body_Retinoic acid treatment

ABSTRACT: S6K1 Knockout mice has a lean phenotype and resitant to a High Fat Diet-induced obesity (Um S.H., Nature, 2004). Adipocyte differentiation consists of two step, first, commitment from stem cell to adipocyte progenitors and second, terminal differentiation from adipocyte progenitors to mature adipocyte. We studied S6K1-dependent gene expression regulation in early stage of commitment by employing ES cell(ESC)-Embryoid Bodies(EBs) differentiation model. We established stable ES cell lines infected with either control non-silencing shRNA (shNS) or S6K1 targetting shRNA (shS6K1). Each sample was treated with retinoic acid for 3 days to induce adipogenesis, then gene expression profile was analyzed employing microarrays and up-regulated and down-regulated genes were selected for analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE20349 | GEO | 2010/02/17

SECONDARY ACCESSION(S): PRJNA125439

REPOSITORIES: GEO

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Mouse_embryoid Body_Retinoic acid treatment

Project description:S6K1 Knockout mice has a lean phenotype and resitant to a High Fat Diet-induced obesity (Um S.H., Nature, 2004). Adipocyte differentiation consists of two step, first, commitment from stem cell to adipocyte progenitors and second, terminal differentiation from adipocyte progenitors to mature adipocyte. We studied S6K1-dependent gene expression regulation in early stage of commitment by employing ES cell(ESC)-Embryoid Bodies(EBs) differentiation model. We established stable ES cell lines infected with either control non-silencing shRNA (shNS) or S6K1 targetting shRNA (shS6K1). Each sample was treated with retinoic acid for 3 days to induce adipogenesis, then gene expression profile was analyzed employing microarrays and up-regulated and down-regulated genes were selected for analysis. Mouse Embryoid Bodies (approximately 1000 EBs per sample) were treated with retinoic acid (1ÂµM) for 3 days then collected for RNA extraction and hybridization on Affimetrix microarray. Two biological replicates were each performed for EBs prepared from either shNS ESCs or shS6K1 ESCs.

2010-05-14 | E-GEOD-20349 | biostudies-arrayexpress

Prediction and Testing of Novel Transcriptional Networks Regulating Embryonic Stem Cell Self-Renewal and Commitment

Project description:We have used mouse embryonic stem cells (ESCs) as a model to study the signaling mechanisms that regulate self-renewal and commitment to differentiation. We hypothesized that genes critical to stem cell fate would be dynamically regulated at the initiation of commitment. Time course microarray analysis following initiation of commitment led us to propose a model of ESC maintenance in which highly regulated transcription factors and chromatin remodeling genes (down-regulated in our time course) maintain repression of genes responsible for cell differentiation, morphogenesis and development (up-regulated in our time course). Microarrays of Oct4, Nanog and Sox2 shRNA knockdown cell lines confirmed predicted regulation of target genes. shRNA knockdowns of candidate genes were tested in a novel high throughput screen of self-renewal, confirming their role in ESC pluripotency. We have identified genes that are critical for self-renewal and those that initiate commitment and developed draft transcriptional networks that control self-renewal and early development. Keywords: genetic modification Gene expression in Oct4 knockdown, Sox2 knockdown and their empty vector contol ES cells was analyzed.

2010-06-11 | E-GEOD-7520 | biostudies-arrayexpress

A genome wide RNAi screen in mouse embryonic stem cells identifies Mp1 as a key mediator of differentiation

Project description:Despite intense investigation of intrinsic and extrinsic factors that regulate pluripotency, the process of initial fate commitment of embryonic stem (ES) cells is still poorly understood. Here, we used a genome wide shRNA screen in mouse ES cells to identify genes that are essential for initiation of differentiation. Knockdown of the scaffolding protein Mek binding protein 1 (Mp1, also known as Lamtor3, Map2k1ip1) stimulated self-renewal of ES cells, blocked differentiation and promoted proliferation. Fibroblast growth factor 4 (FGF4) signaling is required for initial fate commitment of ES cells. Knockdown of Mp1 inhibited FGF4-induced differentiation but did not alter FGF4 driven proliferation. This uncoupling of differentiation and proliferation was also observed when oncogenic Ras isoforms were over expressed in ES cells. Knockdown of Mp1 redirected FGF4 signaling from differentiation towards pluripotency and upregulated the pluripotency-related genes Esrrb, Rex1, Tcl1 and Sox2. We also found that human germ cell tumors express low amounts of Mp1 in the invasive embryonic carcinoma and seminoma histologies and higher amounts of Mp1 in the non-invasive carcinoma in situ precursor and differentiated components. Knockdown of Mp1 in invasive germ cell tumor cells resulted in resistance to differentiation, thereby showing a functional role for Mp1 both in normal differentiation of ES cells as well as in germ cell cancer.

2011-11-15 | GSE32595 | GEO

A genome wide RNAi screen in mouse embryonic stem cells identifies Mp1 as a key mediator of differentiation

2011-11-15 | E-GEOD-32595 | biostudies-arrayexpress

Thermogenic differentiation of adipocyte progenitors

Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2). Time course expression profiling was performed during differentiation. In addition, some cultures of differentiated adipocytes were stimulated with norepinephrine for 3 hours. In parallel, differentiation and norepinephrine stimulation of progenitors from interscapular brown fat was performed and profiled.

2015-08-20 | E-MTAB-3693 | biostudies-arrayexpress

Transcriptional response to Rosiglitazone in adipocyte progenitors isolated from WT and Cited4-KO scWAT

Project description:Lin-Sca-1+ adipocyte progenitors from subcutaneous adipose tissue of wild-type and Cited4-/- female mice were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with Rosi). Cells were harvested 48 post-induction of differentiation.

2018-07-04 | E-MTAB-6796 | biostudies-arrayexpress

Endogenous fluctuations of OCT4 and SOX2 bias pluripotent cell fate decisions

Project description:SOX2 and OCT4 are pioneer transcription factors playing a key role in embryonic stem (ES) cell self-renewal and differentiation. How temporal fluctuations in their expression levels bias lineage commitment is unknown. Here we generated knock-in reporter fusion ES cell lines allowing to monitor endogenous SOX2 and OCT4 protein fluctuations in living cells and to determine their impact on mesendodermal and neuroectodermal commitment. We found that small differences in SOX2 and OCT4 levels impact cell fate commitment in G1 but not in S phase. Elevated SOX2 levels modestly increased neuroectodermal commitment and decreased mesendodermal commitment upon directed differentiation. In contrast, elevated OCT4 levels strongly biased ES cells towards both neuroectodermal and mesendodermal fates. Using ATAC-seq on ES cells gated for different endogenous SOX2 and OCT4 levels, we found that high OCT4 levels increased chromatin accessibility at differentiation-associated enhancers. This suggests that small endogenous fluctuations of pioneer transcription factors can bias cell fate decisions by concentration-dependent priming of differentiation-associated enhancers.

2019-09-23 | GSE126554 | GEO

Genome-wide analysis of gene expression perturbed by Pontin shRNA in MCF7 subjected to normoxic and hypoxic conditions

Project description:In order to investigate the role of Pontin methylation on the expression of hypoxia responsive genes across the whole genome, we performed a microarray analysis from RNAs isolated from MCF7 cells expressing either control shRNA (shNS) or Pontin shRNA(shPontin) in normoxic and hypoxic conditions.

2011-12-02 | GSE27813 | GEO

Jak kinase inhibition in mouse adipocyte progenitors

Project description:FACS-purified adipocyte progenitors from murine subcutaneous adipose tissue were cultured under conditions promoting general adipogenic differentiation or beige/brite adipocyte differentiation (treatment with cPGI2) in the presence of absence of Jak inhibitor I (JakiI), which targets all Jak family members. The cells were harvested 24 hours after induction of differentiation.

2018-04-24 | E-MTAB-6029 | biostudies-arrayexpress

A compound directed against S6K1 hampers fat mass expansion and mitigates diet-induced hepatosteatosis

Project description:Imbalanced mTORC1-S6K1 engages signalling cascades related to obesity and fatty liver. Here, we set up to assess the therapeutic blockage of the ribosomal protein S6 kinase 1 (S6K1) in diet-induced obese (DIO) mice challenged with LY2584702 (LY) tosylate, a specific oral S6K1 inhibitor initially developed for the treatment of solid tumours. To characterize the ability of LY in counteracting obesity and diet-induced disturbances, DIO male mice were challenged every 12 h by oral gavage with LY in treatments lasting 12 and 4 weeks. We show that diminished S6K1 activity in mice treated with LY hampers fat mass expansion and ameliorates dyslipidaemia and hepatic steatosis, while modifying transcriptome-wide gene expression programs relevant for adipose and liver performance. Accordingly, impaired mTORC1 signalling in fat (decreased) and liver (increased) co-segregated with defective epithelial-mesenchymal transition, being prominent a decreased expression of Cd36 (coding for a fatty acid translocase) and Lgals1 (Galectin 1) in both tissues. All these factors combined align with reduced adipocyte size and improved lipidomic signatures, while hypertriglyceridemia and hepatic steatosis were improved in treatments of 12 and 4 weeks. This study provides new insights into the therapeutic intervention of S6K1 signalling, and opens a promising avenue for prevalent metabolic diseases.

2022-08-01 | GSE193028 | GEO

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