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GSE23675
Mus musculus
28 Downloadable Samples
Illumina MouseWG-6 v2.0 expression beadchip
Description
The signaling pathway for Nodal, a ligand of the transforming growth factor-beta (TGF-beta) superfamily, plays a central role in regulating the maintenance and/or differentiation of stem cell types that can be derived from the peri-implantation mouse embryo. Extraembryonic endoderm stem (XEN) cells are derived from the primitive endoderm of the blastocyst, which normally gives rise to the parietal and the visceral endoderm in vivo, but XEN cells do not contribute efficiently to the visceral endoderm in chimeric embryos. We have found that treatment of XEN cells with Nodal and/or Cripto, an EGF-CFC co-receptor for Nodal, results in up-regulation of markers for visceral endoderm as well as anterior visceral endoderm (AVE). Re-introduction of treated XEN cells into chimeric embryos by blastocyst injection or morula aggregation results in contribution to visceral endoderm and AVE. In culture, XEN cells do not express Cripto, but do express the related EGF-CFC co-receptor Cryptic and require Cryptic for Nodal signaling. Notably, the response to Nodal can be blocked by treatment with the ALK4/ALK5/ALK7 inhibitor SB431542, but Cripto treatment is unaffected, suggesting that its activity is independent of type I activin receptors. Gene set enrichment analysis of genome-wide expression signatures generated from XEN cells under these treatment conditions confirms the differing responses of Nodal- and Cripto-treated XEN cells to SB431542. Our findings define distinct pathways for Nodal and Cripto in the differentiation of visceral endoderm and AVE from XEN cells, and provide new insights into the specification of these cell types in vivo.
Publication Title
Regulation of extra-embryonic endoderm stem cell differentiation by Nodal and Cripto signaling.
Sample Metadata Fields
Cell line, Treatment, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
NextSeq 500
Description
Numerous mechanisms to support cells under conditions of transient nutrient starvation have been described. The tumor suppressor protein p53 can contribute to the adaptation of cells to metabolic stress through various mechanisms that may help cancer cell survival in nutrient limiting conditions. We show here that p53 helps cancer cells to survive glutamine starvation by promoting the expression of SLC1A3, an aspartate/glutamate transporter that allows the utilization of aspartate to support cells in the absence of extracellular glutamine. Under glutamine deprivation, SLC1A3 expression maintains electron transport chain and tricarboxylic acid cycle activity, promoting de novo glutamate, glutamine and nucleotide synthesis to rescue cell viability. Tumor cells with high levels of SLC1A3 expression are resistant to glutamine starvation and SLC1A3 depletion retards the growth of these cells in vitro and in vivo, suggesting a therapeutic potential for SLC1A3 inhibition. Overall design: We quantify transcription via high throughput RNA sequencing in HCT116 cells (WT1 and WT2 clones) grown in complete medium (CM) or in glutamine-free medium (GD) for 48 hours.
Publication Title
A Role for p53 in the Adaptation to Glutamine Starvation through the Expression of SLC1A3.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Homo sapiens
- 64 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Purpose: To evaluate the presence of a gene expression signature present before treatment as predictive of response to treatment with MAGEA3
Publication Title
Predictive gene signature in MAGE-A3 antigen-specific cancer immunotherapy.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxd4 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Publication Title
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Homeobox genes of the Hox class are required for proper patterning of skeletal elements and play a role in cartilage differentiation. In transgenic mice with overexpression of Hoxc8 during cartilage development, we observed severe defects, namely physical instability of cartilage, accumulation of immature chondrocytes, and decreased maturation to hypertrophy. To define the molecular basis underlying these defects, we performed gene expression profiling using the Affymetrix microarray platform.
Publication Title
Microarray Analysis of Defective Cartilage in Hoxc8- and Hoxd4-Transgenic Mice.
Sample Metadata Fields
Specimen part
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression.
Sample Metadata Fields
Sex, Disease
View Samples- Caenorhabditis elegans
- 6 Downloadable Samples
- Affymetrix C. elegans Genome Array (celegans)
Description
Here we exploit the essential process of Xchromosome dosage compensation to elucidate basic mechanisms that control the assembly, genomewide binding, and function of gene regulatory complexes that act over large chromosomal territories. We demonstrate that a subunit of C. elegans MLL/COMPASS, a gene-activation complex, acts within the dosage compensation complex (DCC), a condensin complex, to target the DCC to both X chromosomes of hermaphrodites and thereby reduce chromosome-wide gene expression. The DCC binds to two categories of sites on X: rex sites that recruit the DCC in an autonomous, sequence- dependent manner, and dox sites that reside primarily in promoters of expressed genes and bind the DCC robustly only when attached to X. We find that DCC mutants that abolish rex-site binding do not eliminate dox-site binding, but instead reduce it to the level observed at autosomal binding sites in wild-type animals. Changes in DCC binding to these non-rex sites occur throughout development and correlate with transcriptional activity of adjacent genes. Moreover, autosomal DCC binding is enhanced by rex-site binding in cis in X-autosome fusion chromosomes. Thus, dox and autosomal sites exhibit similar binding properties. Our data support a model for DCC binding in which low-level DCC binding at dox and autosomal sites is dictated by intrinsic properties correlated with high transcriptional activity. Sex-specific DCC recruitment to rex sites then greatly elevates DCC binding to dox sites in cis, which lack intrinsically high DCC affinity on their own. We also show here that the C. elegans DCC achieves dosage compensation through its effects on transcription.
Publication Title
An MLL/COMPASS subunit functions in the C. elegans dosage compensation complex to target X chromosomes for transcriptional regulation of gene expression.
Sample Metadata Fields
No sample metadata fields
View Samples- Hordeum vulgare
- 44 Downloadable Samples
- Affymetrix Barley Genome Array (barley1)
Description
Barley cv. Morex inoculated with Fusarium graminearum (isolate Butte 86) or water (mock). Sampled at 24, 48, 72, 96 and 144 hours after treatment. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, Jayanand Boddu. The equivalent experiment is BB9 at PLEXdb.]
Publication Title
Transcriptome analysis of the barley-Fusarium graminearum interaction.
Sample Metadata Fields
Specimen part, Time
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Analysis of the role of PARP1 in gene transcription in MCF7 cells under non-stress conditions. The hypothesis was that PARP1 activity in MCF7 cells plays a role in gene transcription. The results indicate that PARP1 inhibition does not significantly affect transcription after 6 hours of treatment.
Publication Title
Basal activity of a PARP1-NuA4 complex varies dramatically across cancer cell lines.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 12 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Analysis of the role of PARP1 in gene transcription in cell lines with variable PARP1 activity.
Publication Title
Basal activity of a PARP1-NuA4 complex varies dramatically across cancer cell lines.
Sample Metadata Fields
Specimen part, Cell line
View Samples