Project description:Time series expression profile of yeast cells grown at high glucose and shifted to low glucose containing medium. Lowess normalized data in raw data files.
Project description:To assess the diurnal gene expression in gills of oyster Crassotrea gigas, gills of 6 oysters were pooled and analyzed by RNa-seq every 4h for 52h (i.e. 13 sampling times). This procedure was executed simultaneously for control oysters fed with the non-harmful algae Heterocapsa triquetra (H.t condition), and for oysters fed with the harmful algae Alexandrium minutum (A.m condition) (L:D 9:15). Alexandrium minutum exposure led to a remodeling of the cycling transcriptome in gills of Crassostrea gigas.
Project description:Eukaryotic chromatin is separated into functional domains differentiated by posttranslational histone modifications, histone variants, and DNA methylation. Methylation is associated with repression of transcriptional initiation in plants and animals, and is frequently found in transposable elements. Proper methylation patterns are critical for eukaryotic development, and aberrant methylation-induced silencing of tumor suppressor genes is a common feature of human cancer. In contrast to methylation, the histone variant H2A.Z is preferentially deposited by the Swr1 ATPase complex near 5' ends of genes where it promotes transcriptional competence. How DNA methylation and H2A.Z influence transcription remains largely unknown. Here we show that in the plant Arabidopsis thaliana, regions of DNA methylation are quantitatively deficient in H2A.Z. Exclusion of H2A.Z is seen at sites of DNA methylation in the bodies of actively transcribed genes and in methylated transposons. Mutation of the MET1 DNA methyltransferase, which causes both losses and gains of DNA methylation, engenders opposite changes in H2A.Z deposition, while mutation of the PIE1 subunit of the Swr1 complex that deposits H2A.Z17 leads to genome-wide hypermethylation. Our findings indicate that DNA methylation can influence chromatin structure and effect gene silencing by excluding H2A.Z, and that H2A.Z protects genes from DNA methylation. Keywords: Affinity-purification on microarray All experiments were done using two channels per chip. DNA methylation experiments compared immunoprecipitated, methylated DNA to control genomic DNA. H2A.Z experiments compared whole micrococcal nuclease-treated affinity-purified chromatin to input chromatin used for affinity purification. Affinity purification was performed using either biotin-tagged H2A.Z, pulled down using streptavidin, or endogenous H2A.Z pulled down using an anti-H2A.Z antibody.
Project description:This microarray study compared the gene expression profile of rat tail tendon tissue in three different developmental stages: embryonic day 21, postnatal 3 weeks and postnatal 6 weeks.<br><br><br><br>Key words: rat tail tendon, tissue development, embryonic and postnatal
Project description:Galectin-3 (Gal-3) has emerged as a novel RNA-binding protein. Here we applied eCLIP to identify the RNAs bound by Gal-3 in mouse embryonic stem cells differentiated by deprivation of the leukaemia inhibitory factor (LIF) for 7 days.
Project description:We superimposed array comparative genomic hybridization (aCGH) data onto existing expression array profiles (GSE3892) to sift out the pivotal genes underlying the pathogenesis of a well defined series of diffuse large B-cell lymphomas (DLBCL). 280 gained and over-expressed genes were identified, located on chromosomes 1q, 3q, 7, 12p12, 18q and 21q. At the most frequently gained region the oncogene MDMX/MDM4 was concurrently over-expressed, which is a critical regulator of p53 function. In regions of frequent chromosomal loss, 36 genes were concurrently down-regulated, restricted to 6q and 15p. These putative tumor suppressor genes included PERP, MAP3K5, CCNDBP1 and β2M, and loss of 6q was associated with poor clinical outcome. Genes identified and chromosomal regions validated in an independent series of DLBCL patients. Overall design fields: Copy number profiles (array CGH) of a series of 42 Diffuse large B-cell lymphoma patient samples were analyzed a) for frequency of aberrations and b) for impact on gene expression. No duplicate samples or dye-swaps were analyzed. a) Statistical analysis of Array CGH data Calling: Areas of gains and losses and their frequencies throughout the dataset were determined from the Bluefuse ratios within the statistical package â??CGHcallâ?? (van de Wiel et al., 2007). Briefly, after smoothing outliers and median normalization, â??DNAcopyâ?? segmentation (Olshen et al., 2004) was applied within CGHcall, after which a call was assigned to each position on the genome. Within CGHcall the probabilities of the calls were determined per chromosomal arm, and a cellularity correction of 0.75 was applied to each sample because tumor cellularity in all DLBCL is estimated to be maximal 75%, taking into account all stromal, endothelial en infiltrating lymphocytes. After calling, we applied â??CGHregionsâ?? (van de Wiel and van Wieringen 2007) to determine regions of consecutive clones with highly similar calls for all samples. This dimension reduction further increases robustness and statistical power for downstream statistical analyses. Called data were used for all downstream analyses. b) Integration with expression data To integrate called array CGH data with expression array data, the array CGH and expression integration tool, ACE-it (van Wieringen et al., 2006), was used. For ACE-it analysis chromosomal amplifications were included in the gains. ACE-it uses the one-sided Wilcoxon rank sum to test which chromosomal aberrations recurrently affect RNA expression and adjust p-values for multiple testing. Only those clones were taken into account which had at least 20% (9) of the samples in one of the other calling states (gain or loss). Only genes were considered relevant with a false discovery rate of <0.1. References - Olshen AB, Venkatraman ES, Lucito R, Wigler M (2004) Circular binary segmentation for the analysis of array-based DNA copy number data. Biostatistics 5: 557-72. - van de Wiel MA, Kim KI, Vosse SJ, van Wieringen WN, Wilting SM, Ylstra B (2007) CGHcall: calling aberrations for array CGH tumor profiles. Bioinformatics 23: 892-4. - van de Wiel MA, van Wieringen WN. CGHregions: dimension reduction for array CGH data with minimal information loss. Cancer Informatics. In press 2007. - van Wieringen WN, Belien JA, Vosse SJ, Achame EM, Ylstra B (2006) ACE-it: a tool for genome-wide integration of gene dosage and RNA expression data. Bioinformatics 22: 1919-20.
Project description:Aside from the perinatal complications associated with low birth weight, individuals born with intra-uterine growth restriction suffer from chronic diseases late in life that ultimately lead to a shortened lifespan. These late life metabolic sequelae of low birth weight include obesity and metabolic syndrome, diabetes mellitus, cardiovascular disease, hypertension, stroke, dyslipidemia, and non-alcoholic fatty liver disease/steatohepatitis. Animal models employing perinatal calorie restriction recapitulate the observations made in humans. Interestingly, if continued calorie restriction is employed post-natally the late life sequelae of intra-uterine growth restriction are ameliorated. These observations linking both fetal and early post natal growth to later health is now termed the developmental origins of health and disease. To further our understanding of the mechanism of how early growth affects late life health we have employed Affymetrix microarray-based expression profiling to characterize hepatic gene expression in a rat model of maternal semi-nutrient restriction. In these experiments we have limited maternal calorie intake to 50% of normal so as to create 3 groups of animals: Control (Con) male offspring born to mothers who were fed normally throughout gestation and lactation; intra-uterine calorie restricted male offspring (IUCR) born to mothers who had 50% restriction of calories from e11 to e21; and combined intra-uterine and post-natal calorie restriction (IPCR) male offspring who were born to mothers who received calorie restriction during both fetal growth (e11 to e21) and post-natally (p1-p21). Livers were collected at p21(day 21 of life) for Con and IPCR groups (IUCR withheld owing to ‘catch up” growth), and at p450 (day 450 of life) for Con, IUCR, and IPCR. The profiling data reveals clear alteration of circadian cycling at P21, and subtle changes for circadian gene expression at p450. In addition, a clear transcriptional response is found during active calorie restriction at p21 but an absence of a transcriptional response late in life at p450. Transcritional studies have been performed using Affymetrix Rat Gene 1.0 arrays for the following treatment groups, with each group run in triplicate (each replicate from separate littermates): Day 21 Control, Day 21 IPCR, Day 450 Con, Day 450 IUCR, Day 450 IPCR
Project description:Acting in a partially redundant manner, NF-Ys were shown previously to regulate bacterial infection, including selection of a superior rhizobial strain, and to participate in mediating nodule structure formation. However, the exact mechanism(s) by which these transcriptional factors exert their symbiotic functions has remained elusive. Gene expression profiling for wild-type and Nuclear Factor YA (nf-ya)-A mutants in roots of Lotus japonicus were conducted 4 days after inoculation with Mesorhizobium loti in order to understand the interaction of NF-Ys and other genes in Lotus japonicus.