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GSE55372
Saccharomyces cerevisiae
17 Downloadable Samples
Affymetrix Yeast Genome S98 Array (ygs98)
Description
Diurnal temperature cycling is an intrinsic characteristic of many exposed microbial ecosystems. However, its influence on yeast physiology and transcriptome has not been studied in detail. In this study, 24-h sinoidal temperature cycles, oscillating between 12 and 30C, were imposed on anaerobic, glucose-limited chemostat cultures of Saccharomyces cerevisiae. After three diurnal temperature cycles (DTC), concentrations of glucose, and extracellular metabolites, as well as CO2-production rates showed regular, reproducible circadian rhytms. DTC also led to waves of transcriptional activation and repression, which involved one sixth of the yeast genome. A substantial fraction of these DTC-responsive genes appeared to primarily respond to changes in glucose concentration. Elimination of known glucose-responsive genes revealed overrepresentation of previously identified temperature-responsive genes as well as genes involved in cell cycle and de novo purine biosynthesis. Analyses of budding index and flow cytomery demonstrated that DTC led to a partial synchronization of the cell cycle of the yeast populations in the chemostat cultures, which was lost upon release from DTC. Comparison of DTC results with data from steady-state cultures showed that DTC was sufficiently slow to allow S. cerevisiae chemostat cultures to almost completely acclimatize their transcriptome and physiology at the DTC temperature maximum, and to approach acclimation at the DTC temperature minimum.
Publication Title
Physiological and transcriptional responses of anaerobic chemostat cultures of Saccharomyces cerevisiae subjected to diurnal temperature cycles.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 6 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Systemic transcriptional responses in Arabidopsis thaliana distal leaves to wounding
Publication Title
The plant NADPH oxidase RBOHD mediates rapid systemic signaling in response to diverse stimuli.
Sample Metadata Fields
Age, Specimen part
View Samples- Danio rerio
- 6 Downloadable Samples
IlluminaHiSeq2500
Description
We report gene expression data for FACS sorted zebrafish mpeg1:mCherry + and mpx:EGFP + cells collected from whole embryos at 72 hours post fertilization (hpf). We also report gene expression data for the remaining, transgene negative, portion of these embryos. Overall design: ~1,000 mpeg1:mCherry+; mpx:EGFP+ transgenic embryos were homogenized, filtered, and sorted using FACS into PBS, collecting >50,000 cells for each of the three populations: mpeg1:mCherry+, mpx:EGFP+ and double negative (no double positive cells were collected as there was almost no overlap between mCherry and EGFP expression).
Publication Title
Distinct Roles for Matrix Metalloproteinases 2 and 9 in Embryonic Hematopoietic Stem Cell Emergence, Migration, and Niche Colonization.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 21 Downloadable Samples
- Illumina HiSeq 2000
Description
Angioimmunoblastic T-cell lymphoma (AITL) is an aggressive lymphoid tumor derived from malignant transformation of T follicular helper (Tfh) cells. Genetically, AITL is characterized by loss of function mutations in the Ten-Eleven Translocation 2 (TET2) epigenetic tumor suppressor and a highly recurrent mutation (p.Gly17Val, G17V) in the RHOA small GTPase gene Moreover, RHOA G17V expression in Tet2 deficient hematopoietic progenitors resulted in the specific development of lymphoid tumors resembling human AITL. Notably, inhibition of ICOS signaling impaired the growth of RHOA G17V-induced mouse lymphomas in vivo, thus providing a potential new rational approach for the treatment of AITL. Overall design: We analyzed mRNA expression profiles of primary tumor cells expressing Rhoa G17V or Rhoa wild type.
Publication Title
RHOA G17V Induces T Follicular Helper Cell Specification and Promotes Lymphomagenesis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 3 Downloadable Samples
- Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
We analyzed the generation of mouse gliomas following the overexpression of PDGF-B in embryonic neural progenitors. Comparison of our microarray data, with published gene expression data sets for many different murine neural cell types, revealed a closest relationship between our tumor cells and oligodendrocyte progenitor cells, confirming definitively that PDGF-B-induced gliomas are pure oligodendrogliomas.
Publication Title
PDGF-B induces a homogeneous class of oligodendrogliomas from embryonic neural progenitors.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 18 Downloadable Samples
- Affymetrix Mouse Gene 2.1 ST Array (mogene21st)
Description
To investigate the impact of the iNKT cells on the tumor-infiltrating leukocytes in TRAMP mouse prostate cancer.
Publication Title
Bimodal CD40/Fas-Dependent Crosstalk between iNKT Cells and Tumor-Associated Macrophages Impairs Prostate Cancer Progression.
Sample Metadata Fields
Age, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Illumina Genome Analyzer
Description
Coordinated BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. Persistence of oncogenic p27 functions despite effective inhibition of BCR-ABL1 may contribute to resistance to tyrosine kinase inhibitors. Overall design: BCR-ABL1 induced p27 versus knockout, controlling with Empty vector p27 versus knock out
Publication Title
BCR-ABL1 promotes leukemia by converting p27 into a cytoplasmic oncoprotein.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Illumina HumanWG-6 v3.0 expression beadchip
Description
DNA methylation, histone modifications, and nucleosomal occupancy collaborate to cause silencing of tumor related genes in cancer. The development of drugs that target these processes is therefore important for cancer therapy. Inhibitors of DNA methylation and histone deacetylation have already been approved by the FDA for the treatment of hematologic malignancies. However, drugs that target the other mechanisms still need to be developed. Recently, 3-deazaneplanocin A (DZNep) was reported to selectively inhibit the trimethylation of lysine 27 on histone H3 (H3K27me3) and lysine 20 on histone H4 (H4K20me3) as well as re-activate silenced genes in cancer cells. This finding opens the door to pharmacological inhibition of histone methylation and we therefore wanted to further study the mechanism of action of 3-deazaneplanocin A in cancer cells. Western blot analysis showed that two other drugs, sinefungin and adenosine-dialdehyde (Adox), have similar effects on the trimethylation H3K27 as 3-deazaneplanocin A and that DZNep is not selective, but globally inhibits histone methylation. Intriguingly, chromatin immunoprecipitation of various histone modifications and microarray analysis show DZNep acts via a different pathway to 5-aza-2-deoxycytidine (5-azaCdR), a DNA methyltransferase inhibitor and gives us an interesting insight into how chromatin structure effects gene expression. We also determine the kinetics of gene activation in order to understand if the induced changes were somatically heritable. We have found that upon removal of DZNep, gene expression is reduced to its original state suggesting that there is a homeostatic mechanism which returns the histone modifications to their ground state after DZNep treatment. Not only do these studies show the strong need for further development of histone methylation inhibitors but also allow us to better understand how chromatin structure affects gene expression.
Publication Title
DZNep is a global histone methylation inhibitor that reactivates developmental genes not silenced by DNA methylation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
- Illumina human-6 v2.0 expression beadchip
Description
DNA methylation, histone modifications, and nucleosomal occupancy collaborate to cause silencing of tumor related genes in cancer. The development of drugs that target these processes is therefore important for cancer therapy. Inhibitors of DNA methylation and histone deacetylation have already been approved by the FDA for the treatment of hematologic malignancies. However, drugs that target the other mechanisms still need to be developed. Recently, 3-deazaneplanocin A (DZNep) was reported to selectively inhibit the trimethylation of lysine 27 on histone H3 (H3K27me3) and lysine 20 on histone H4 (H4K20me3) as well as re-activate silenced genes in cancer cells. This finding opens the door to pharmacological inhibition of histone methylation and we therefore wanted to further study the mechanism of action of 3-deazaneplanocin A in cancer cells. Western blot analysis showed that two other drugs, sinefungin and adenosine-dialdehyde (Adox), have similar effects on the trimethylation H3K27 as 3-deazaneplanocin A and that DZNep is not selective, but globally inhibits histone methylation. Intriguingly, chromatin immunoprecipitation of various histone modifications and microarray analysis show DZNep acts via a different pathway to 5-aza-2-deoxycytidine (5-azaCdR), a DNA methyltransferase inhibitor and gives us an interesting insight into how chromatin structure effects gene expression. We also determine the kinetics of gene activation in order to understand if the induced changes were somatically heritable. We have found that upon removal of DZNep, gene expression is reduced to its original state suggesting that there is a homeostatic mechanism which returns the histone modifications to their ground state after DZNep treatment. Not only do these studies show the strong need for further development of histone methylation inhibitors but also allow us to better understand how chromatin structure affects gene expression.
Publication Title
DZNep is a global histone methylation inhibitor that reactivates developmental genes not silenced by DNA methylation.
Sample Metadata Fields
Cell line
View Samples- Mus musculus, Homo sapiens
- 10 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling.
Sample Metadata Fields
Specimen part
View Samples