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GSE7536
Mus musculus
64 Downloadable Samples
Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)
Description
The inner ear in mammals is derived from a simple ectodermal thickening called the otic placode. Through a series of complex morphological changes, the placode forms the mature inner ear comprising of the auditory organ (cochlea) and the vestibular/balance organs (utricle, saccule, and three semi-circular canals). The vast majority of genes known to be involved during inner ear development have been found through mutational screens or by chance.
Publication Title
Toward a systems biology of mouse inner ear organogenesis: gene expression pathways, patterns and network analysis.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 22 Downloadable Samples
Illumina HiSeq 2000
Description
A molecular and bioinformatic pipeline permitting comprehensive analysis and quantification of myocardial miRNA and mRNA expression with next-generation sequencing was developed and the impact of enhanced PI3Kalpha signaling on the myocardial transcriptome signature of pressure overload-induced pathological hypertrophy was explored. Overall design: miRNA and mRNA-Seq were carried out in four groups of mouse LV samples: WT sham, WT+TAC, caPI3Kalpha sham, caPI3Kalpha+TAC
Publication Title
Combined deep microRNA and mRNA sequencing identifies protective transcriptomal signature of enhanced PI3Kα signaling in cardiac hypertrophy.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Several transcription factors are known to be expressed in discrete regions of the otic vesicle and Dlx5 is one of those that is expressed highly in the presumptive dorsal vestibular region. Mice lacking Dlx5 have vestibular defects. Specifically, they fail to form the endolymphatic duct (a defect visible as early as E10) as well as the anterior and posterior semi-circular canals. The lateral canal does form but is smaller, whereas the saccule, the utricle and the cochlea appear relatively normal. The goal of this study was to use microarrays to identify differentially expressed genes between wild-type and Dlx5-null otic vesicles microdissected from E10 and 10.5 and identify downstream targets of Dlx5 by searching the immediate 3kb promoter regions of the differentially expressed genes for homeodomain binding sites followed by chromatin immunoprecipitation in an otic vesicle-derived cell line over-expressing Dlx5.
Publication Title
Identification of direct downstream targets of Dlx5 during early inner ear development.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 40 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Temporal- and strain-specific host microRNA molecular signatures associated with swine-origin H1N1 and avian-origin H7N7 influenza A virus infection.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 40 Downloadable Samples
- Illumina HumanHT-12 V3.0 expression beadchip
Description
MicroRNAs (miRNAs) repress the expression levels of genes by binding to mRNA transcripts, acting as master regulators of cellular processes. Differential expression of miRNAs has been linked to viral-associated diseases involving members of the hepacivirus, herpesvirus, and retrovirus families. In contrast, limited biological and molecular information has been reported on the potential role of cellular miRNAs in the lifecycle of influenza A viruses (infA). In this study, we hypothesize that elucidating the miRNA expression signatures induced by low-pathogenic swine-origin influenza A virus (S-OIV) pandemic H1N1 (2009) and highly pathogenic avian-origin (A-OIV) H7N7 (2003) infections could reveal temporal and strain-specific miRNA fingerprints during the viral lifecycle, shedding important insights into the potential role of cellular miRNAs in host-infA interactions. Using a microfluidic microarray platform, we profiled cellular miRNA expression in human A549 cells infected with S- and A-OIVs at multiple time-points during the viral lifecycle, including global gene expression profiling during S-OIV infection. Using target prediction and pathway enrichment analyses, we identified the key cellular pathways associated with the differentially expressed miRNAs and predicted mRNA targets during infA infection, including immune system, cell proliferation, apoptosis, cell cycle, and DNA replication and repair. By identifying the specific and dynamic molecular phenotypic changes (microRNAome) triggered by S- and A-OIV infection in human cells, we provide experimental evidence demonstrating a series of temporal- and strain-specific host molecular responses involving different combinatorial contributions of multiple cellular miRNAs. Our results also identify novel potential exosomal miRNA biomarkers associated with pandemic S-OIV and deadly A-OIV-host infection.
Publication Title
Temporal- and strain-specific host microRNA molecular signatures associated with swine-origin H1N1 and avian-origin H7N7 influenza A virus infection.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 30 Downloadable Samples
- Illumina HiSeq 1500
Description
Embryonic stem (ES) cells have a remarkable capacity to self-organize complex, multi-layered optic cups in vitro via a culture technique called SFEBq. During both SFEBq and in vivo optic cup development, Rax (Rx) expressing neural retina epithelial (NRE) tissues utilize Fgf and Wnt/ß-catenin signalling pathways to differentiate into neural retina (NR) and retinal-pigmented epithelial (RPE) tissues, respectively. How these signaling pathways affect gene expression during optic tissue formation has remained largely unknown, especially at the transcriptome scale. Overall design: We generated Day 10 Rx+ optic tissue using SFEBq, exposed these tissues to either Fgf or Wnt/ß-catenin stimulation, and assayed their gene expression at Days 12 and 15 using RNA-Seq. We measured gene expression in these 5 sample groups in biological triplicate using RNA-seq (Illumina HiSeq) .
Publication Title
Comparative, transcriptome analysis of self-organizing optic tissues.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 9 Downloadable Samples
- IlluminaHiSeq2000
Description
Identify genes that are differentially regulated as a consequence of restoration of full-length functional APC in a colorectal cancer cell lines. Overall design: Examine mRNA expression level changes between SW480 (APC defective) and SW480+APC (SW480 cells with restored functional APC) cells, whilst accounting for any non-specific expression changes by comparison to SW480+control vector.
Publication Title
Differential RNA-seq analysis comparing APC-defective and APC-restored SW480 colorectal cancer cells.
Sample Metadata Fields
No sample metadata fields
View Samples- Drosophila melanogaster
- 9 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Nutrient-responsive oogenesis in Drosophila is a complex and dynamic process regulated, in part, by members of the Pc and Trx complexes. The recent finding that O-GlcNAc Transferase (ogt/sxc) is essential for Pc repression raises the question of whether this nutrient-sensing pathway plays a role in regulating oogenesis. OGT transfers O-GlcNAc to key transcriptional regulators in response to graded levels of the nutrient-derived precursor UDP-GlcNAc; O-GlcNAcase (OGA) catalyzes the removal of O-GlcNAc. Here we produced a null allele of oga (oga1) in Drosophila to examine its in vivo function. We found that oga mutant flies were viable, but that females displayed greatly reduced fecundity. The ovaries from the female OGA knockout exhibited a starvation-like phenotype, even under well-fed conditions. Germline stem cell division was slowed in the germarium of OGA knockout fly ovarioles. Ovaries from the oga1 mutants displayed significantly decreased H3K4 monomethylation in germline stem cells. The Trithorax family members Trx and Ash1 and Compass member Set1 histone methyltransferases are O-GlcNAc modified in oga1 mutant ovaries. Our results suggest that the loss of OGA disrupts oogenesis at least in part by interfering with H3K4 monomethylation in germ cells in the ovary. The findings also suggest that O-GlcNAc cycling is an essential part of the nutrient-responsive epigenetic machinery regulating Drosophila oogenesis in response to a changing nutrient supply.
Publication Title
Drosophila O-GlcNAcase Deletion Globally Perturbs Chromatin O-GlcNAcylation.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 125 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Epipolymorphisms associated with the clinical outcome of autoimmune arthritis affect CD4+ T cell activation pathways.
Sample Metadata Fields
Sex
View Samples- Homo sapiens
- 125 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Multifactorial diseases, including autoimmune juvenile idiopathic arthritis (JIA), result from a complex interplay between genetics and environment. Epigenetic mechanisms are believed to integrate such gene-environment interactions, fine-tuning gene expression and possibly contributing to immune system dysregulation. Although anti-TNF therapy has strongly increased JIA remission rates, it is not curative and up to 80% of patients flare upon treatment withdrawal. Thus, a crucial unmet medical and scientific need is to understand the immunological mechanisms associated with remission or flare to inform clinical decisions. Here, we explored the CD4+ T cell DNA methylome of 68 poly-articular and extended oligo-articular JIA patients, before and after anti-TNF therapy withdrawal, to identify features associated with maintenance of inactive disease (ID). Individual CpG sites were clustered in coherent modules without a priori knowledge of their function through network analysis. The methylation level of several CpG modules, specifically those enriched in CpG sites belonging to genes that mediate T cell activation, uniquely correlated with clinical activity. Differences in DNA methylation were already detectable at the time of therapy discontinuation, suggesting epigenetic predisposition. RNA profiling also detected differences in T cell activation markers, including HLA-DR, but, overall, its sensitivity was lower than epigenetic profiling. Changes to the T cell activation signature at the protein level were detectable by flow cytometry, confirming the biological relevance of the observed alterations in methylation. Our work proposes, for the first time, epigenetic discrimination between clinical activity states, and reveals T cell-related biological functions tied to, and possibly predicting and/or causing, clinical outcome.
Publication Title
Epipolymorphisms associated with the clinical outcome of autoimmune arthritis affect CD4+ T cell activation pathways.
Sample Metadata Fields
Sex
View Samples