Maternal environment is an important regultor of seed dormancy, but the mechanisms underlying the process are poorly understood. We have found that genes in the circadian clock control dormancy, in part through their regulation of the canonical photoperiod pathway known from research into flowering time control. In this experiment we compare the affects of altering seed maturation temperature or maternal photoperiod on dry seed transcriptomes, and the photoperiod-insenstive ft-1 mutant to wt type Ler. In this way we are identifying gene expression programmes which result from the seed's response to maternal environmental experience.
Induction of dormancy in Arabidopsis summer annuals requires parallel regulation of DOG1 and hormone metabolism by low temperature and CBF transcription factors.
Specimen part
View SamplesPurpose: Investigate cellular heterogeneity in a fresh human ovarian cancer tissue sample Methods: Enzymatic digestion of fresh tissue sample collected from the operating room to produce single cell suspension. Cells were labelled with fluorescent antibodies to CD3, CD14, CD19, CD20, CD56 and FACS sorted to remove immune cells. The negative population was used for sequencing. Single cells were processed using the Fluidigm C1 Chip to generate barcoded cDNA for each cell. Amplifed cDNA was sequenced using an Illumina HiSeq 2500 machine. Results: Single cell RNA sequence data was obtained for 92 cells and a "bulk" sample of 1000 cells. 26 cells were removed from analysis due to quality control standards. The remaining 66 cells and the bulk sample were analyzed. Conclusion: Single cell RNA sequence analysis reveals heterogeneity in gene expression in cells harvested from a high grade ovarian serous cancer Overall design: A single cell suspension generated from a fresh high grade serous ovarian cancer sample was run through two Fluidigm C1 chips to isolate single cells and produce barcoded cDNA. Sequencing was performed in a single lane of an Illumina HiSeq 2500 machine. 92 single cells were sequenced and 1 bulk sample was sequenced, for a total of 93 samples.
Single cell sequencing reveals heterogeneity within ovarian cancer epithelium and cancer associated stromal cells.
Subject
View SamplesExpression quantitative trait loci (eQTL) analyses were conducted separately on the glomerular and tubular portions of healthy human kidney samples obtained from subjects of European descent. Overall design: We aimed to define genotype driven gene expression changes in the glomerular and tubular compartments of human kidneys, identifying genetic variants (eVariants) that influence the expression of genes (eGenes). Later, we integrated this information with genotype and phenotype association studies (GWAS) to identify genes for which expression in the kidney shows differences in patients with GWAS variants.
Mapping eGFR loci to the renal transcriptome and phenome in the VA Million Veteran Program.
Specimen part, Disease, Disease stage, Subject
View SamplesPurpose:To identify resistance mechanisms for the chemotherapeutic drug fludarabine in chronic lymphocytic leukemia (CLL), as innate and acquired resistance to fludarabine-based chemotherapy represents a major challenge for long-term disease control. Methods: We employed piggyBac transposon-mediated mutagenesis, combined with next-generation sequencing, to identify genes that confer resistance to fludarabine in a human CLL cell line. Results: RNA-seq profiling of fludarabine-resistant cells suggested deregulated MAPK signaling as involved in mediating drug resistance in CLL. Overall design: To address if the fludarabine-resistant HG3 cells were transcriptionally different at a global level compared to their parental cells, we performed RNA-sequencing of three pairs of HG3 pools
Transposon Mutagenesis Reveals Fludarabine Resistance Mechanisms in Chronic Lymphocytic Leukemia.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.
Specimen part, Cell line
View SamplesGene-expression in siRNA treated U2OS and hTERT-RPE1 cells showed that CASP8AP2, NPAT and HINFP do not regulate expression of each other, and do not have any common target genes, except histones. Most histone genes are downregulated in U2OS cells following loss of CASP8AP2, NPAT or HINFP. In normal cells, highly-expressed histone genes were downregulated, albeit less than in tumor cells following loss of CASP8AP2. The p53 target genes were upregulated relatively late, clearly after the changes in expression of histone genes were observed.
Genome-wide screen of cell-cycle regulators in normal and tumor cells identifies a differential response to nucleosome depletion.
Cell line
View SamplesTGR5 (Gpbar1) is a G protein-coupled receptor responsive to bile acids (BAs), which is expressed in different non-parenchymal cells of the liver, including biliary epithelial cells, liver-resident macrophages, sinusoidal endothelial cells (LSECs) and activated hepatic stellate cells (HSCs). Mice with targeted deletion of TGR5 are more susceptible towards cholestatic liver injury induced by cholic acid-feeding and bile duct ligation, resulting in a reduced proliferative response and increased liver injury. Conjugated lithocholic acid (LCA) represents the most potent TGR5 BA ligand and LCA-feeding has been used as a model to rapidly induce severe cholestatic liver injury in mice. Thus, TGR5 knockout (KO) mice and wildtype littermates were fed a diet supplemented with 1%LCA for 84 hours. Liver injury and gene expression changes induced by the LCA-diet revealed an enrichment of pathways associated with inflammation, proliferation and matrix remodelling. Knockout of TGR5 in mice caused upregulation of endothelin-1 (ET-1) expression in the livers. Analysis of TGR5-dependent ET-1 signalling in isolated LSECs and HSCs demonstrated that TGR5 activation reduces ET-1 expression and secretion from LSECs and triggers internalization of the ET-1 receptor in HSCs dampening ET-1 responsiveness. Thus, we identified two independent mechanisms by which TGR5 inhibits ET-1 signalling and modulates portal pressure.
The G Protein-Coupled Bile Acid Receptor TGR5 (Gpbar1) Modulates Endothelin-1 Signaling in Liver.
Sex
View SamplesMultiple sclerosis is a chronic, inflammatory, demyelinating disease of the central nervous system in which macrophages and microglia play a central role. During active multiple sclerosis foamy macrophages and microglia, containing degenerated myelin, are abundantly found in demyelinated areas. Recent studies have described an altered macrophage phenotype after myelin internalization. However, by which mechanisms myelin affects the phenotype of macrophages and how this phenotype can influence lesion progression is unclear.
Myelin-derived lipids modulate macrophage activity by liver X receptor activation.
Specimen part, Treatment
View SamplesBackground: Global gene expression profiling has been widely used in lung cancer research to identify clinically relevant molecular subtypes as well as to predict prognosis and therapy response. So far, the value of these multi-gene signatures in clinical practice is unclear and the biological importance of individual genes is difficult to assess as the published signatures virtually do not overlap.
Biomarker discovery in non-small cell lung cancer: integrating gene expression profiling, meta-analysis, and tissue microarray validation.
Sex, Age
View SamplesThe ACBP knockout were created by targeted disruption of the gene in mice. The expression profiling was performed on liver tissue from ACBP-/- (KO) and +/+ (WT) mice at the age of 21 days, which in our study is the time immediately before weaning. The mice used for this experiment were taken directly away from their mother. Thus, having free access to chow and breast milk until sacrificed at 8-11am
Disruption of the acyl-CoA-binding protein gene delays hepatic adaptation to metabolic changes at weaning.
Specimen part
View Samples