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GSE8902
Saccharomyces cerevisiae
8 Downloadable Samples
Affymetrix Yeast Genome S98 Array (ygs98)
Description
Previously, it has been demonstrated that formate can be utilized by Saccharomyces cerevisiae as additional energy source using cells grown in a glucose-limited chemostat. Here, we investigated utilization of formaldehyde as co-substrate. Since endogenous formaldehyde dehydrogenase activities were insufficient to allow co-feeding of formaldehyde, the Hansenula polymorpha FLD1, encoding formaldehyde dehydrogenase, was introduced in S. cerevisiae. Chemostat cultivations revealed that formaldehyde was co-utilized with glucose, but the yield was lower than predicted. Moreover, formate was secreted by the cells. Upon co-expression of the H. polymorpha gene encoding formate dehydrogenase, FMD, the levels of secreted formate decreased, but the biomass yield was still lower than anticipated.
Publication Title
Engineering and analysis of a Saccharomyces cerevisiae strain that uses formaldehyde as an auxiliary substrate.
Sample Metadata Fields
No sample metadata fields
View Samples- Saccharomyces cerevisiae
- 11 Downloadable Samples
- Affymetrix Yeast Genome S98 Array (ygs98)
Description
Extremely low specific growth rates (below 0.01 h-1) represent a largely unexplored area of microbial physiology. Retentostats enable controlled, energy-limited cultivation at near-zero specific growth rates while avoiding starvation. In this study, anaerobic, glucose-limited retentostats were used to analyze physiological and genome-wide transcriptional responses of Saccharomyces cerevisiae to cultivation at near-zero specific growth rates. Cultures at near-zero specific growth rates exhibited several characteristics previously associated with quiescence, including accumulation of storage polymers and an increased expression of genes involved in storage metabolism, autophagy and exit from the replicative cell cycle into G0. Analysis of transcriptome data from glucose-limited retentostat and chemostat cultures showed, as specific growth rate was decreased, quiescence-related transcriptional responses already set in at specific growth rates above 0.025 h-1. Many genes involved in mitochondrial processes were specifically upregulated at near-zero specific growth rates, possibly reflecting an increased turn-over of organelles under these conditions. Prolonged (> 2 weeks) cultivation in retentostat cultures led to induction of several genes that were previously implicated in chronological ageing. These observations stress the need for systematic dissection of physiological responses to slow growth, quiescence, ageing and starvation and indicate that controlled cultivation systems such as retentostats can contribute to this goal.
Publication Title
Cellular responses of Saccharomyces cerevisiae at near-zero growth rates: transcriptome analysis of anaerobic retentostat cultures.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mesenchymal progenitor cells can be differentiated in vitro into myotubes that exhibit many characteristic features of primary mammalian skeletal muscle fibers. However, in general, they do not show the functional excitation-contraction coupling or the striated sarcomere arrangement typical of mature myofibers. Epigenetic modifications have been shown to play a key role in regulating the progressional changes in transcription necessary for muscle differentiation. In this study, we demonstrate that treatment of murine C2C12 mesenchymal progenitor cells with 10 M of the DNA methylation inhibitor 5-azacytidine (5AC) promotes myogenesis, resulting in myotubes with enhanced maturity as compared to untreated myotubes. Specifically, 5AC treatment resulted in the upregulation of muscle genes at the myoblast stage while at later stages nearly 50 % of the 5AC-treated myotubes displayed a mature, well-defined sarcomere organization as well as spontaneous contractions that coincided with action potentials and intracellular calcium transients. Both the percentage of striated myotubes and their contractile activity could be inhibited by 20 nM TTX, 10 M ryanodine and 100 M nifedipine, suggesting that action potential-induced calcium transients are responsible for these characteristics. Our data suggest that genomic demethylation induced by 5AC overcomes an epigenetic barrier that prevents untreated C2C12 myotubes from reaching full maturity.
Publication Title
Epigenetics: DNA demethylation promotes skeletal myotube maturation.
Sample Metadata Fields
Cell line, Treatment
View Samples- Homo sapiens
- 7 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
CD141+DNGR-1+ cDC1 have a dual origin. Both MLP and CMP can differentiate in CD141+DNGR-1+ cDC1s.
Publication Title
Dendritic Cell Lineage Potential in Human Early Hematopoietic Progenitors.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 23 Downloadable Samples
Illumina HiSeq 2000
Description
Human lung adenocarcinoma exhibits a propensity for de-differentiation, which complicates diagnosis and treatment, and predicts for poor overall patient survival. In genetically engineered mouse (GEM) models of lung cancer, expression of the BRAFV600E oncoprotein kinase initiates the growth of benign tumors that retain characteristics of their cell of origin, alveolar type II (ATII) pneumocytes. Cooperating genetic alterations such as silencing of the PTEN tumor suppressor or expression of mutationally-activated PI3-kinase-a (PIK3CAH1047R) promote malignant progression of such benign tumors to malignant adenocarcinoma, though their effects on differentiation status are unknown. To address this in vivo, we generated a new conditional BrafCAT allele in which Cre-mediated recombination leads to expression of a bi-cistronic mRNA encoding both BRAFV600E and the tdTomato fluorescent protein. Using this model, we demonstrate that coincident expression of BRAFV600E and PIK3CAH1047R in ATII pneumocytes leads to rapid and widespread cell de-differentiation. Surprisingly, the combined effects of BRAFV600E and PIK3CAH1047R on ATII pneumocyte identity occurred without loss of expression of the lung lineage transcription factors NKX2.1, FOXA1, or FOXA2. Instead, we demonstrate a novel role of PGC1a in maintaining pneumocyte identity, which is lost upon PIK3CAH1047R expression. These findings provide additional insight into how two of the most commonly mutated growth factor signaling pathways contribute to the pathogenesis of lung adenocarcinoma. Overall design: BRAFV600E mutant mouse lung adenocarcinoma (n=6) vs BRAFV600E;PIK3CAH1047R mutant lung adenocarcinoma (n= 8), and BRAFV600E;PGC1aHET (n=5) vs BRAFV600E;PGC1aNULL tumors (n=4)
Publication Title
Mutationally-activated PI3'-kinase-α promotes de-differentiation of lung tumors initiated by the BRAF<sup>V600E</sup> oncoprotein kinase.
Sample Metadata Fields
Sex, Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
beta-glucan induced glycolysis in HIF-1 depedent manner. We reported that beta-glucan injection in mice led to upregulated glycolysis. HIF-1a plays a major role in this process. Overall design: Mice receives beta-glucan via ip for 4 days. Splenocytes were isolated for RNA sequencing.
Publication Title
mTOR- and HIF-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina HiSeq 2500
Description
We aimed to determine the characteristic of IL-10-producing ILCs induced from ILC2s by RA. We found that IL-10-producing ILCs has distinct characteristic compared to IL-10 negative ILCs. Overall design: mRNA profile of IL-10 positive ILCs and IL-10 negative ILCs genarated from ILC2s
Publication Title
A novel proangiogenic B cell subset is increased in cancer and chronic inflammation.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
To identify the CD4+ T cell cytokines responsible for the proliferation of the Lin-IEL lines CD4+ T cell clone L10, which recognises DQ2-glia-1, one of the immunodominant T cell epitopes in celiac disease, was stimulated for 3 hours in IMDM with plate-bound CD3/CD28-specific (2.5 g/ml each) or control antibodies coated onto 6-well non-tissue culture treated plates. Three independent biological replicates were performed, each time including 6 million Ficoll-purified live cells per condition. RNA was purified from these cells using the RNAeasy mini kit (Qiagen, Venlo, the Netherlands). cDNA was amplified using the Applause WT-Amp system (NuGEN technologies, Bemmel, the Netherlands) and biotin-labelled with the Encore Biotin Module (NuGEN). Human Gene 1.0 ST arrays (Affymetrix, High Wycombe, UK) were employed to quantify global gene expression.
Publication Title
CD4 T-cell cytokines synergize to induce proliferation of malignant and nonmalignant innate intraepithelial lymphocytes.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Inflammation-induced repression of chromatin bound by the transcription factor Foxp3 in regulatory T cells.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
The transcription factor Foxp3 is indispensable for the ability of regulatory T (Treg) cells to suppress fatal inflammation. Here, we characterized the role of Foxp3 in chromatin remodeling and regulation of gene expression in actively suppressing Treg cells in an inflammatory setting. Although genome-wide Foxp3 occupancy of DNA regulatory elements was similar in resting and in vivo activated Treg cells, Foxp3-bound enhancers were poised for repression only in activated Treg cells. Following activation, Foxp3-bound sites showed reduced chromatin accessibility and selective H3K27 tri-methylation, which was associated with Ezh2 recruitment and downregulation of nearby gene expression. Thus, Foxp3 poises its targets for repression by facilitating formation of repressive chromatin in regulatory T cells upon their activation in response to inflammatory cues.
Publication Title
Inflammation-induced repression of chromatin bound by the transcription factor Foxp3 in regulatory T cells.
Sample Metadata Fields
Specimen part
View Samples