We used a chicken RNA microarray to identify differentially expressed genes in order to compare two layer lines kept in a small group housing system Eurovent Deutsch.
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Specimen part
View SamplesUsing HiSeq2000 to sequence white leghorn different parts (ovary, magnum, isthmus and uterus) of oviduct at 40-weeks.
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View SamplesIdentification of candidate genes for drip loss
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Sex, Specimen part
View SamplesTo study the splicing factor role of ZmGRP1
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Sex, Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesPig RNA-seq.
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View SamplesCuticular wax is a major composition of plant surface cuticle, which exerts crucial functions in optimizing plant growth. Histone acetylation regulates gene expression of diverse biological processes, but little is known about its role in cuticular wax synthesis. Here we observed that mutation of Arabidopsis histone acetyltransferase GCN5 gene impaired stem cuticular wax accumulation. Furthermore, three target genes of GCN5 (CER3, CER26 and CER1-L1) were identified by RNA-Seq and ChIP assays. Consistently, H3K9/14 acetylation levels in promoter regions of CER3, CER26 and CER1-L1 were significantly decreased in gcn5 as compared to wild type. Notably, overexpression of CER3 in the gcn5 mutant restored the stem cuticular wax accumulation. Collectively, these data demonstrate that Arabidopsis GCN5 is involved in stem cuticular wax accumulation by modulating CER3 expression via H3K9/14 acetylation, which present evidence that histone acetylation plays an important role in cuticular wax biosynthesis
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Specimen part
View SamplesInsulin resistance represents a hallmark during the development of type 2 diabetes mellitus (T2D) and in the pathogenesis of obesity-associated disturbances of glucose and lipid metabolism 1,2,3. MicroRNA (miR)-dependent posttranscriptional gene silencing has recently been recognized to control gene expression in disease development and progression including that of insulin-resistant T2D. MiRs, whose deregulation alters hepatic insulin sensitivity include miR-143, miR-181 and miR-103/107. Here we report that expression of miR-802 is increased in liver of two obese mouse models and of obese human subjects. Inducible transgenic overexpression of miR-802 in mice causes impaired glucose tolerance and attenuates insulin sensitivity, while reduction of miR-802 expression improves glucose tolerance and insulin action. We identify Hnf1b as a target of miR-802-dependent silencing and shRNA-mediated reduction of Hnf1b in liver causes glucose intolerance, impairs insulin signaling and promotes hepatic gluconeogenesis. In turn, hepatic overexpression of Hnf1b improves insulin sensitivity in db/db mice. Thus, the present study defines a critical role for deregulated expression of miR-802 in the development of obesity-associated impairment of glucose metabolism via targeting Hnf1b and assigns Hnf1b an unexpected role in the control of hepatic insulin sensitivity.
Obesity-induced overexpression of miR-802 impairs glucose metabolism through silencing of Hnf1b.
Sex, Specimen part
View SamplesTranscriptome of connective tissue of swine affected and non-affected with scrotal hernia
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Sex, Age, Specimen part, Disease
View SamplesUrechis unicinctus, a benthic marine worm inhabiting widely in the coast of Russia, Japan, Korean Peninsula and China, present special biological characteristics in morphology, reproductive and developmental biology as well as physiology. It could exist in condition of low oxygen, high sulfide and pollution where most animals could not live. However, the molecular mechanisms of resistance are still unknown and the main obstacle to further study is the limited genomic and genetic information. In order to improve the situation, we performed and acquired its transcriptome database.
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View SamplesThe aim of this study is to analyze the transcriptome of epithelial (CD326+ enriched) and immune (CD45+ enriched) fraction in Celiac Disease and controls to find differentially expressed genes.
The methylome of the celiac intestinal epithelium harbours genotype-independent alterations in the HLA region.
Sex, Age, Specimen part, Disease
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