Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA310119 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3132650_1.fastq.gz | Fastqsanger.gz | |||
| SRR3132650_2.fastq.gz | Fastqsanger.gz | |||
| SRR3132651_1.fastq.gz | Fastqsanger.gz | |||
| SRR3132651_2.fastq.gz | Fastqsanger.gz | |||
| SRR3132648_1.fastq.gz | Fastqsanger.gz |
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Project description:We constructed a polycistronic lentiviral vector to overexpress 3 germ cell specific genes (Stella, Oct4 and Nanos2) in mouse embryonic fibroblast (MEFs) and evaluated the transcriptome portrait in partially reprogrammed cells.We sequenced RNA samples from bulk cell population of two biological duplicates of MEF-GFP (control) and MEF-SON (overexpressed) 21 days post infection. Differential expression analysis of 50 M pair-end read per samples showed overexpression of neurogenesis, blood vessel and proliferation related genes and downregulation of chondroitin sulphate metabolic process, nitric oxide production and innate immune response genes. Examination of whole transcriptome following concurrent overexpression of Stella, Oct4 and Nanos2 in MEFs.
2016-07-30 | E-GEOD-77351 | biostudies-arrayexpress
Project description:We constructed a polycistronic lentiviral vector to overexpress 3 germ cell specific genes (Stella, Oct4 and Nanos2) in mouse embryonic fibroblast (MEFs) and evaluated the transcriptome portrait in partially reprogrammed cells.We sequenced RNA samples from bulk cell population of two biological duplicates of MEF-GFP (control) and MEF-SON (overexpressed) 21 days post infection. Differential expression analysis of 50 M pair-end read per samples showed overexpression of neurogenesis, blood vessel and proliferation related genes and downregulation of chondroitin sulphate metabolic process, nitric oxide production and innate immune response genes.
2016-07-30 | GSE77351 | GEO
Project description:Human embryonic stem cells (hESCs) harbor the ability to undergo lineage-specific differentiation into clinically relevant cell types. Transcription factors and epigenetic modifiers are known to play important roles in the maintenance of pluripotency of hESCs. However, little is known about regulation of pluripotency through splicing. In this study, we identify the spliceosome-associated factor SON as a novel factor essential for the maintenance of hESCs. Depletion of SON in hESCs results in the loss of pluripotency and cell death. Using genome-wide RNA profiling, we identified transcripts that are regulated by SON. Importantly, we confirmed that SON regulates the proper splicing of transcripts encoding for pluripotency regulators such as PRDM14, OCT4, E4F1 and MED24. Furthermore, we show that SON is bound to these transcripts in vivo. In summary, we connect a splicing-regulatory network for accurate transcription production to the maintenance of pluripotency and self-renewal of hESCs.
2013-08-29 | E-MTAB-1687 | biostudies-arrayexpress
Project description:Next Generation Sequencing with differdent pluripotent transcript factor overexpression in MEF Somatic cells can be reprogrammed into induced pluripotent stem cells (iPSCs) by defined factors. The low efficiency of reprogramming limited the potential application of iPSCs. Here we found that knockdown LSD1 , which demethylates histone H3 Lys 4 or 9 , could increase iPSCs generation. It has been reported that LSD1 interaction with Oct4 which is the core factor of reprogramming. So we try to find out the different of overexpression Oct4 or Kllf4/Sox2 in MEF and LSD1 inhibitor. Retrovirus-mediated different pluripotent transcript factor overexpression in MEF cells after 4 days collect mRNA profiles processing with Illumina MiSeq; MEF, Mouse Embryonic Fibroblast O, MEF infected with Oct4 KS,MEF infected with Klf4 and Sox2 OSK, MEF infected with Oct4 Klf4 and Sox2 T20, MEF infected with Oct4 Klf4 and Sox2 and treated with 20nm LSD1 inhibitor Tranylcypromine
2015-09-17 | E-GEOD-61694 | biostudies-arrayexpress
Project description:To elucidate the function of NANOS2 to regulate the transcriptome in embryonic male germ cells, we performed expression microarray analysis of the embyornic gonads of the Nanos2+/-, Nanos2-/- male and wild type female from E12.5 to E15.5. The Nanos2+/- and Nanos2-/- female gonads at E15.5 were analyzed as a negative control.
2013-02-06 | GSE37716 | GEO
Project description:Spermatogonial stem cells are foundation of spermatogenesis. In our previous study, we observed a rapid degeneration of spermatogenesis by conditional knockout (cKO) of Nanos2 in adult spermatogonia, but the underlying mechanisms are largely unknown. While, conditional overexpression (cOE) of Nanos2 also inhibited germ cell development and stayed in undifferentiation status. Here we used cultured germline stem cells (GSCs) to study the mechanisms of Nanos2 in spermatogonia. We compared Nanos2 expression in cultured GSCs with in vivo isolated Nanos2 positive cells, and found the level of Nanos2 is significantly lower in GSCs as compared to Nanos2 positive cells. Thus we generated Nano2 cOE GSCs lines. By conditional inducing expression of Nanos2 we compared gene expression profile to control GSCs. These data provide the first evidence of Nanos2 regulating genes in spermatogonial stem cells.
2015-09-25 | GSE61808 | GEO
Project description:To elucidate the function of NANOS2 to regulate the transcriptome in embryonic male germ cells, we performed expression microarray analysis of the embyornic gonads of the Nanos2+/-, Nanos2-/- male and wild type female from E12.5 to E15.5. The Nanos2+/- and Nanos2-/- female gonads at E15.5 were analyzed as a negative control. Biological duplicates were examined at each stage, genotype, and sex for each experiment.
2013-02-06 | E-GEOD-37716 | biostudies-arrayexpress
Project description:Differentiated cells can be reprogrammed into induced pluripotent stem cells (iPSCs) following the forced overexpression of a specific combination of transcription factors, of which Oct4 is essential. To better understand the mechanism underlying iPSC reprogramming, we investigated the immediate transcriptional response to ectopic Oct4 expression in somatic cells. To this end, we derived different somatic cell types from Oct4-inducible transgenic mice and induced Oct4 expression for different time periods. Using microarray analysis, we have identified early transcriptional Oct4 targets, including genes not previously known to interact with Oct4. Comparison of the sets of Oct4-regulated genes revealed pronounced differences among the individual cell types. Furthermore, a notable up-regulation of pluripotent markers could not be detected. In contrast, we observed a down-regulation of somatic markers specific to each cellular population. This finding suggests that Oct4 interferes with the somatic transcriptional program in a cell type-specific manner, thereby promoting an unstable epigenetic state that facilitates reprogramming rather than the direct initiation of a pluripotent gene expression network. Finally, we show that Mgarp, a gene expressed in pluripotent cells, is commonly up-regulated in all cell types after Oct4 induction. Unexpectedly, Mgarp expression decreases during the first steps of reprogramming due to a Klf4-dependent inhibition. Our data show that Oct4 counteracts Klf4 repressive activity and enhances Mgarp expression at the late stages of reprogramming. This temporal pattern of Mgarp expression is crucial for the efficient generation of iPSCs. In summary, our study provides new insights into the specific role that Oct4 plays during the early stages of reprogramming. Different somatic cell types were derived from transgenic mice containing both a tetracycline-inducible transactivator (rtTA-M2) and a tetracycline operon-controlled Oct4 expression cassette (TO) (Hochedlinger 2005, Cell 121:465-477) that were mated with GOF18-GFP mice in which the green fluorescent protein (GFP) is driven by 18 kb of the Oct4 regulatory region (Oct4-GFP) (Yoshimizu 1999, Dev Growth Differ 41:675-684), thus indicating endogenous Oct4 expression. In addition, a control neural stem cell (CtrlNSC) line was generated from transgenic mice that entail a tetracycline-inducible transactivator (irtTA-VP16-GBD) (Anastassiadis 2002, Gene 298:159-172) plus an OG2 Oct4-GFP reporter transgene (Yoshimizu 1999),but lack a TO cassette. A second control consisted of wild type (C57BL/6) mouse embryonic fibroblasts (CtrlMEF). Oct4-inducible mouse embryonic fibroblasts (TO-MEFs) and neural stem cell (TO-NSCs) were derived from 14.5 days post coitum (d.p.c.) embryos and cultured as previously described (Conti 2005, PLoS Biol 3:e283). Primary bone marrow cells (TO-BMCs) were isolated from 6-week old mice after flushing femora and tibiae and plated onto dishes with a combined coating of gelatin (PAA, Pasching, Austria), laminin (Santa Cruz Biotechnology, Santa Cruz, CA), and poly-L-lysine (Sigma, St. Louis, MO). Adherent cells were then cultivated in DMEM Low Glucose (Gibco, Carlsbad, CA) with 10% fetal bovine serum, 100 U/ml penicillin, 100 µg/ml streptomycin, and 2 mM/L glutamine (all PAA). The transgenic Oct4 expression was induced by either 6 µg/ml doxycycline (Sigma) or by 2 µg/ml doxycycline (Dox) plus 10–7 M dexamethasone (Sigma), depending on the respectively contained tetracycline transactivator. 5-azacytidine (10 nM, Sigma) and cycloheximide (30 µg/ml, Sigma) were applied as indicated. Generation, culture, and differentiation of ESCs and iPSCs were performed as previously described (Tiemann 2011, Cytometry A 79:426-435). Microarray Gene Expression Analysis Samples from Oct4-inducible cell types and controls were collected at different time points (0, 6, 12, and 24 hours after induction). Biotin-labeled cRNA was prepared with the linear TotalPrep RNA Amplification Kit (Ambion, Austin, TX) from 500 ng original RNA and hybridized onto MouseRef 8 v2.0 Expression BeadChips (Illumina, San Diego, CA). The chips were stained with streptavidin-Cy3 (GE Healthcare, Little Chalfont, UK) and scanned using the iScan reader (Illumina). Bead intensities were mapped to gene information using BeadStudio 3.2 (Illumina) and background correction was performed using the Affymetrix robust multiarray analysis model. Variance stabilization was performed by log2 scaling and the R-Bioconductor lumi package was used for normalization. 17 samples were analyzed. ESC: Mouse Embryonic Stem Cell (ESC) TO_MEF_0: Tetracycline Oct4 (TO) Mouse Embryonic Fibroblast (MEF), time 0h TO_MEF-6: Tetracycline Oct4 (TO) Mouse Embryonic Fibroblast (MEF), time 6h TO_MEF-12: Tetracycline Oct4 (TO) Mouse Embryonic Fibroblast (MEF), time 12h TO_MEF-24: Tetracycline Oct4 (TO) Mouse Embryonic Fibroblast (MEF), time 24h TO_BMC-0: Tetracycline Oct4 (TO) Mouse Bone Marrow Cell (BMC), time 0h TO_BMC-6: Tetracycline Oct4 (TO) Mouse Bone Marrow Cell (BMC), time 6h TO_BMC-12: Tetracycline Oct4 (TO) Mouse Bone Marrow Cell (BMC), time 12h TO_BMC-24: Tetracycline Oct4 (TO) Mouse Bone Marrow Cell (BMC), time 24h TO_NSC-0: Tetracycline Oct4 (TO) Mouse Neural Stem Cell (NSC), time 0h TO_NSC-6: Tetracycline Oct4 (TO) Mouse Neural Stem Cell (NSC), time 6h TO_NSC-12: Tetracycline Oct4 (TO) Mouse Neural Stem Cell (NSC), time 12h TO_NSC-24: Tetracycline Oct4 (TO) Mouse Neural Stem Cell (NSC), time 24h Ctrl_MEF_0: Control wild type Mouse Embryonic Fibroblast (MEF) untreated Ctrl_MEF_24: Control wild type Mouse Embryonic Fibroblast (MEF) 24h treated Ctrl_NSC_0: Control wild type Mouse Neural Stem Cell (NSC) untreated Ctrl_NSC_24: Control wild type Mouse Neural Stem Cell (NSC) 24h treated
2014-05-13 | E-GEOD-47061 | biostudies-arrayexpress
Project description:Transgenic StellaGFP ESCs were used to derive primordial germ cells during embryoid body (EB) differentiation, and microarry analysis used to compared FACS sorted Stella-positive cells of day 7 Ebs with the parental ESCs and Stella-negative cells of day 7 Ebs. Keywords: in vitro, primordial germ cells, embryonic stem cells, stella
2009-06-22 | GSE7948 | GEO
Project description:Dysregulation of MLL complex-mediated histone methylation plays a pivotal role in gene expression associated with diseases, but little is known about cellular factors modulating MLL complex activity. Here, we report that SON, previously known as an RNA splicing factor, controls MLL complex-mediated transcriptional initiation. SON binds to DNA near transcription start sites, interacts with menin, and inhibits MLL complex assembly, resulting in decreased H3K4me3 and transcriptional repression. Importantly, alternatively spliced short isoforms of SON are markedly upregulated in acute myeloid leukemia. The short isoforms compete with full-length SON for chromatin occupancy, but lack the menin-binding ability, thereby antagonizing full-length SON function in transcriptional repression while not impairing full-length SON-mediated RNA splicing. Furthermore, overexpression of a short isoform of SON enhances replating potential of hematopoietic progenitors. Our findings define SON as a fine-tuner of the MLL-menin interaction and reveal short SON overexpression as a marker indicating aberrant transcriptional initiation in leukemia.
2016-03-24 | GSE76910 | GEO