The Arabidopsis thaliana defense regulator EDM2 was previously shown to be specifically required for disease resistance to the pathogenic oomycete Hyaloperonospora parasitica aradidopsis mediated by the R protein RPP7. We found EDM2 to have a promoting effect on several distinct developmental processes, such as leaf pavement cell development, vegetative phase change or the floral transition. We further identified the atypical protein kinase WNK8 to physically interact with EDM2 in nuclei.
Co-option of EDM2 to distinct regulatory modules in Arabidopsis thaliana development.
Specimen part
View SamplesWe performed a global analysis of both miRNAs and mRNAs expression across sixteen human cell lines and extracted negatively correlated pairs of miRNA and mRNA which indicate miRNA-target relationship. The many of known-target of miR-124a showed negative correlation, suggesting our analysis were valid. We further extracted physically relevant miRNA-target gene pairs, applying computational target prediction algorism with inverse correlations of miRNA and mRNA expression. Furthermore, Gene Ontology-based annotation and functional enrichment analysis of the extracted miRNA-target gene pairs indicated putative functions of miRNAs.
Global correlation analysis for micro-RNA and mRNA expression profiles in human cell lines.
No sample metadata fields
View SamplesMicroRNAs are small non-coding RNA species, some of which are playing important roles in cell differentiation. However, the level of participations of microRNAs in epithelial cell differentiation is largely unknown. Here, we found that expression levels of four microRNAs (miR-210, miR-338-3p, miR-33a and miR-451) were significantly increased in differentiated stage of T84 cells, compared with undifferentiated stage. Additionally, we demonstrate that miR-338-3p and miR-451 contribute to the formation of epithelial basolateral polarity by facilitating translocalization of beta1 integrin to the basolateral membrane. However, candidate target mRNAs of miR-338-3p and miR-451 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms.
MicroRNA-338-3p and microRNA-451 contribute to the formation of basolateral polarity in epithelial cells.
Cell line, Treatment, Time
View SamplesRationale Electroconvulsive seizure (ECS) therapy is a nonchemical treatment for depression. Since ECS up-regulates expression of c-Fos in the paraventricular nucleus of hypothalamus (PVN), the function of which is frequently influenced in depression, we hypothesized that ECS modulates functions of the PVN and contributes to its antidepressant effects. Objectives To identify gene expression changes in the mouse PVN by ECS treatment Material and methods First, we established a method to amplify nucleotides from small quantities of RNA. Mice received one shock of ECS and their brains were collected at 2 or 6 h after shock. The PVN was microdissected from dehydrated brain sections, its total RNA was extracted and microarray analysis was applied. Results At 2 h after ECS, 2.6% (589 genes) of the probes showed more than 2-fold decrease, and 0.9% (205 genes) showed more than 2-fold increase. To confirm the expression changes, genes showing differential expression with a wide range in the microarray were analyzed by qPCR. Among the genes with more than 2-fold change by ECS, down-regulated 94 genes and up-regulated 24 genes have been reported the association with anxiety, bipolar disorder or mood disorder by the Ingenuity knowledge database. The groups of down-regulated genes, which are suggested to modulate the function of the PVN or associate to psychiatric disorders, include neuropeptides (Cck), kinases (Prkcb, Prkcc, Camk2a), transcription factors (Bcl6, Tbr1), transporters (Aqp4) and others (Fmr1). Conclusion The present results indicate that ECS treatment can modulate the functions of PVN via a series of gene expression changes, and may contribute to its antidepressant effects at least in part.
Electroconvulsive seizure-induced changes in gene expression in the mouse hypothalamic paraventricular nucleus.
Specimen part, Treatment, Time
View SamplesCircadian clock oscillation emerges in mouse embryo in the later developmental stages. Although circadian clock development is closely correlated with cellular differentiation, the mechanisms of its emergence during mammalian development are not well understood. Here, we demonstrate an essential role of the post-transcriptional regulation of Clock subsequent to the cellular differentiation for the emergence of robust circadian clock oscillation in mouse fetal hearts and mESCs (mouse embryonic stem cells). In mouse fetal hearts, no apparent oscillation of cell-autonomous molecular clock was detectable in around embryonic day (E) 10 whereas robust oscillation was clearly visible in E18 heart. Temporal RNA-seq analysis using mouse fetal hearts reveals much fewer rhythmic genes in E10-12 hearts (63, no clock genes) than E17-19 (483 genes), indicating the lack of functional circadian clocks in E10 mouse fetal hearts. In both mESCs and E10 embryos, CLOCK protein was absent despite the expression of Clock mRNA, which we showed was at least partially due to miRNA-mediated translational suppression of CLOCK. The CLOCK protein is required for the robust molecular oscillation in differentiated cells, and the post-transcriptional regulation of Clock plays a key role in setting the timing for the emergence of the circadian clock oscillation during mammalian development.
Involvement of posttranscriptional regulation of <i>Clock</i> in the emergence of circadian clock oscillation during mouse development.
No sample metadata fields
View SamplesWe used microarrays to select the genes associated glioma patients survival.
Gene expression signature-based prognostic risk score in patients with glioblastoma.
Sex, Age, Disease, Disease stage
View SamplesAnalysis of hepatic gene expression in mice transiently overexpressing Bcl2 Overall design: 3 control GFP mice and 5 GFP-Bcl2 mice, 8 mouse liver samples total
Bcl2 is a critical regulator of bile acid homeostasis by dictating Shp and lncRNA H19 function.
No sample metadata fields
View SamplesA transcription factor Nkx2-1 (also known as TTF-1) regulates the expression of different sets of genes. Gene expression analysis was performed using mRNAs from Nkx2-1-induced A549 cells compared to that from the control A549 cells. We used microarrays to detail the global program of gene expression controlled by Nkx2-1 and identified distinct classes of up-regulated and down-regulated genes.
Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.
Cell line
View SamplesTransgenic mice (Scgb1a1-rtTA/[tetO]-KRAS.G12D/Nkx2-1+/-) develop mucinous lung tumors. Gene expression analysis was performed using mRNAs from the whole lungs of the mice compared to that of the control mice.
Kras(G12D) and Nkx2-1 haploinsufficiency induce mucinous adenocarcinoma of the lung.
Specimen part
View SamplesThe molecular mechanism by which lncRNAs derived from the promoter region where the transcriptional machinery is assembled regulate the expression of neighboring genes during cell differentiation is largely unknown. Myogenesis process has been studied as a model of cell differentiation. Using this model, we found a novel lncRNA, Myoparr, expressed from the promoter region of myogenin gene, one of the regulators of myogenesis. We show that Myoparr regulates the expression of myogenin in vitro and in vivo. In addition, we identified Ddx17 and hnRNPK as Myoparr-binding-proteins. We compared the Transcriptome profiles of C2C12 cells (mouse myoblast cell line) with or without siRNAs against myogenin, Myoparr, Ddx17, and hnRNPK during myogenesis.
Data describing the effects of depletion of <i>M</i><i>yoparr</i>, <i>myogenin</i>, <i>Ddx17</i>, and <i>hnRNPK</i> in differentiating C2C12 cells.
Specimen part, Cell line
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