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GSE27626
Zea mays
12 Downloadable Samples
Affymetrix Maize Genome Array (maize)
Description
Phytophthora cinnamomi is a devastating soil-borne oomycete with a very broad host range however there remains a major gap in the understanding of plant resistance responses to the pathogen, furthermore, necrotrophic plant-pathogen interactions, particularly those of root pathogens, remain poorly understood. Zea mays exhibits non-host resistance to the pathogen and has been well characterised as a model species. Using the maize Affymetrix GeneChip array we conducted genome-wide gene expression profiling to elucidate the defence genes and pathways which are induced in the root tissue of a resistant plant species to the pathogen.
Publication Title
Transcriptional profiling of Zea mays roots reveals roles for jasmonic acid and terpenoids in resistance against Phytophthora cinnamomi.
Sample Metadata Fields
Specimen part, Time
View Samples- Mus musculus
- 57 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Norrin, frizzled-4, and Lrp5 signaling in endothelial cells controls a genetic program for retinal vascularization.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Transcriptional profiles of the cerebellar endothelial cells from P16 Fz4-/- animals were compared to their wild type littermate controls. The goal is to characterize the long-term effect on the transcriptome of loss of Fz4 signaling in cerebellar endothelial cells.
Publication Title
Norrin, frizzled-4, and Lrp5 signaling in endothelial cells controls a genetic program for retinal vascularization.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 23 Downloadable Samples
- Affymetrix Human Genome U133A Array (hgu133a)
Description
Pulmonary hypoxia is a common complication of chronic lung diseases leading to the development of pulmonary hypertension. The underlying sustained increase in vascular resistance in hypoxia is a response unique to the lung. Thus, we hypothesised that there are genes whose expression is altered selectively in the lung in response to alveolar hypoxia.
Publication Title
Lung-selective gene responses to alveolar hypoxia: potential role for the bone morphogenetic antagonist gremlin in pulmonary hypertension.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 16 Downloadable Samples
Illumina HiSeq 2500
Description
G9a mediates a transcriptional switch, and activates the Notch pathway to coordinate endothelial cell and trophoblast proliferation to promote vascular maturation in the placenta. Overall design: Examination of global transcriptional profiles in control and mutant placenta labyrinth at 2 developmental stages (E12.5 and 13.5).
Publication Title
G9a controls placental vascular maturation by activating the Notch Pathway.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Illumina HiSeq 2000
Description
Increasing evidence supports a role for altered gene expression in mediating the lasting effects of cocaine on the brain, and recent work has demonstrated the involvement of chromatin modifications in these alterations. However, all such studies to date have been restricted by their reliance on microarray technologies which have intrinsic limitations. Here, we used advanced sequencing methods, RNA-seq and ChIP-seq, to obtain an unprecedented view of cocaine-induced changes in gene expression and associated adaptations in numerous modes of chromatin regulation in the nucleus accumbens, a key brain reward region. We identify unique combinations of chromatin changes, or signatures, that accompany cocaine’s regulation of gene expression, including the dramatic involvement of pre-mRNA alternative splicing in cocaine action. Together, this delineation of the cocaine-induced epigenome in the nucleus accumbens reveals several novel modes of drug regulation, thereby providing new insight into the biological basis of cocaine addiction. More broadly, the combinatorial chromatin and transcriptional approaches that we describe serve as an important resource for the field, as they can be applied to other systems to reveal novel transcriptional and epigenetic mechanisms of neuronal regulation. Overall design: Total RNA was isolated from mouse nucleus accumbens 24 hr after 7 day daily cocaine or saline control ip injection for mRNA sequencing by following illumina RNA seq kit protocol. Another batch of acute cocaine RNA-seq was performed using the same parameters except the treatment group was given 6 days of saline injection followed by 1 day of cocaine injection. The acute cocaine batch serves as control experiments.
Publication Title
Chronic cocaine-regulated epigenomic changes in mouse nucleus accumbens.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
Description
Many cancers are postulated to harbor developmental hierarchies in which cells display variability in stem-like character, tumor propagating ability, and proliferation. In glioblastoma (GBM), glioma stem cells (GSCs) reside atop such a tumor cellular hierarchy, and are thought to resist current therapies and thus underlie inevitable relapse. Here we show that GSCs can evade RTK inhibition by reversibly regressing to a slow-cycling state reminiscent of quiescent neural stem cells. This process involves up-regulation of numerous histone demethylases, including KDM6A/B, which remodel the chromatin landscape and are selectively essential for drug persister survival. Chromatin remodeling is accompanied by activation of various neurodevelopmental master regulators and Notch signaling, changes which closely parallel critical aspects of neural stem cell biology. Thus our findings illustrate how cancer cells may hijack native developmental programs for deranged proliferation, adaptation, and tolerance in the face of stress. Our studies highlight key roles for chromatin remodeling and developmental plasticity in GBM biology, and suggest strategies for overcoming therapeutic resistance by targeting epigenetic and developmental pathways. Overall design: ChIP-seq for histone modifications and Notch factors in glioblastoma stem cell lines with various drug treatments RNA-seq in glioblastoma stem cell lines with various drug treatments
Publication Title
Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 6 Downloadable Samples
- Illumina Genome Analyzer II
Description
Here we show that Tet1 is down-regulated in mouse nucleus accumbens (NAc), a key brain reward structure, by repeated cocaine administration which enhances behavioral responses to cocaine. Through genome-wide 5hmC profiling, we identified 5hmC changes selectively clustered in both enhancer and coding regions of genes with several annotated neural functions. By coupling with mRNA sequencing, we found cocaine-induced alterations in 5hmC correlate positively with alternative splicing. We also demonstrated that 5hmC alteration at certain genes lasts up to a month after cocaine exposure. Overall design: RNA Nac samples were collected at various time points after 7 daily cocaoine ip administration for 5hmC and transcriptome analysis
Publication Title
Role of Tet1 and 5-hydroxymethylcytosine in cocaine action.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 19 Downloadable Samples
Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Homo sapiens
- 15 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
SUMMARY Despite numerous genome-wide association studies involving glioblastoma (GBM), few therapeutic targets have been identified for this disease. Using patient derived glioma sphere cultures (GSCs), we have found that a subset of the proneural (PN) GSCs undergo transition to a mesenchymal (MES) state in a TNFa/NFkB dependent manner with an associated enrichment of CD44 sub-populations and radio-resistant phenotypes. To the contrary, MES GSCs exhibit constitutive NFkB activation, CD44 enrichment and radio-resistance. Patients whose tumors exhibit a higher MES metagene, increased expression of CD44, or activated NFkB were associated with poor radiation response and shorter survival. Our results indicate that NFkB activation mediated MES differentiation and radiation resistance presents an attractive therapeutic target for GBM.
Publication Title
Mesenchymal differentiation mediated by NF-κB promotes radiation resistance in glioblastoma.
Sample Metadata Fields
Specimen part
View Samples