Bluestem transcription profiles - Konza 2005
Ontology highlight
ABSTRACT:
ORGANISM(S): Andropogon gerardii
SUBMITTER: Steve Travers
PROVIDER: E-GEOD-16418 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We measured transcriptional profiles of individuals of Andropogon gerardii and Sorghastrum nutans, two C4 grass species native to North American grasslands, in a field experiment in which both temperature and precipitation have been manipulated to simulate key aspects of forecasted climate change. 99 samples were analyzed.
2012-05-11 | E-GEOD-35492 | biostudies-arrayexpress
Project description:This study presents statistical analyses of gene expression during all 40 developmental stages in the teleost Fundulus heteroclitus using four biological replicates per stage. Patterns of gene expression for 7,000 genes appear to be important as they recapitulate developmental timing. Among the 45% of genes with significant expression differences between pairs of temporally adjacent stages, significant differences in gene expression vary from as few as five to more than 660. Five adjacent stages have disproportionately more significant changes in gene expression (>200 genes) relative to other stages: four to eight and eight to sixteen cell stages, onset of circulation, pre- and post-hatch, and during complete yolk absorption. The fewest differences among adjacent stages occur during gastrulation. Yet, at stage 16 (pre-mid-gastrulation), the largest number of genes has peak expression. This stage has an over-representation of genes in oxidative respiration and protein expression (ribosomes, translational genes and proteases). Unexpectedly, among all ribosomal genes, both strong positive and negative correlations occur. Similar correlated patterns of expression occur among all significant genes. These data provide statistical support for the temporal dynamics of developmental gene expression during all stages of vertebrate development. A double-loop design was used for the microarray hybridizations, where each sample is hybridized to 2 arrays using both Cy3- and Cy5-labelled fluorophores (Kerr and Churchill 2001a; Kerr and Churchill 2001b). The loop consisted of Cy3- and Cy5-labelled embryo aRNAs from 4 biological pools for each of 40 stages (S). In total, 160 biological pools were hybridized to 80 microarrays. Each array had different combinations of biological pools (Altman and Hua 2006). The double loop formed was S1M-bM-^FM-^R S2 M-bM-^FM-^R S3M-bM-^FM-^R M-bM-^@M-& S40M-bM-^FM-^R S1 and S40M-bM-^FM-^R S39M-bM-^FM-^R S38M-bM-^FM-^R M-bM-^@M-& S2M-bM-^FM-^R S1 M-bM-^FM-^R S40, where each arrow represents a separate hybridization (array) with the biological pool at the base of the arrow labeled with Cy3 and the biological pool at the head of the arrow labelled with Cy5.
2011-04-19 | E-GEOD-21372 | biostudies-arrayexpress
Project description:This study explores the synergistic effects of two model PAHs, an aryl hydrocarbon receptor (AHR) agonist (M-NM-2-naphthoflavone) and a cytochrome P4501A (CYP1A) inhibitor (M-NM-1-naphthoflavone), on gene expression in stage 31 embryos from two different population. One population (Elizabeth River population) is relatively resistant to the pollutants in its environment. A loop design (Figure 5) was used for the microarray hybridizations where each sample is hybridized to 2 arrays using both Cy3 and Cy5 labeled fluorophores (Kerr and Churchill, 2001). The loop consisted of Cy3 and Cy5 labeled embryo aRNAs from 4 biological samples and six different treatments (T1-T6: control, 1 M-NM-<g/L BNF, 50 M-NM-<g/L ANF, 100 M-NM-<g/L ANF, 1 M-NM-<g/L BNF + 50 M-NM-<g/L ANF, 1 M-NM-<g/L BNF + 100 M-NM-<g/L ANF). In total, 48 biological samples were hybridized to 24 microarrays. Each array had different combinations of biological samples, so that the most direct comparisons (i.e., 50 M-BM-5g/L ANF resistant embryo and 50 M-BM-5g/L sensitive embryo) are hybridized to the same array. The loop formed was T1SM-bM-^FM-^R T1R M-bM-^FM-^R T2SM-bM-^FM-^R T2R M-bM-^FM-^RT3SM-bM-^FM-^R T3RM-bM-^FM-^R T4SM-bM-^FM-^R T4RM-bM-^FM-^R T5SM-bM-^FM-^R T5R M-bM-^FM-^R T6SM-bM-^FM-^RT6RM-bM-^FM-^R T1SM-bM-^FM-^R T2S M-bM-^FM-^R T3S M-bM-^FM-^R T4S M-bM-^FM-^R T5S M-bM-^FM-^R T6S M-bM-^FM-^R T1S M-bM-^FM-^R T1R M-bM-^FM-^R T2R M-bM-^FM-^R T3R M-bM-^FM-^R T4R M-bM-^FM-^R T5R M-bM-^FM-^R T6R, where each arrow represents a separate hybridization (array) with the biological sample at the base of the arrow labeled with Cy3 and the biological pool at the head of the arrow labeled with Cy5. T1-6 is treatment, and S and R represent sensitive and resistant embryos.
2013-09-30 | E-GEOD-47654 | biostudies-arrayexpress
Project description:This study presents statistical analyses of gene expression in 5, 10 and 15 day post-fertilization (dpf) embryos of the teleost Fundulus heteroclitus treated with control vehicle (DMSO) or a potent non-ortho-PCB (PCB-126; 3,3’,4,4’,5-pentachlorobiphenyl). The embryos were from two populations: a clean, reference population (SC, Scorton Creek, MA USA) and a polluted Superfund population (N, New Bedford Harbor, MA USA). For each site, eggs from 8 females (~1100 total) were fertilized using minced testes from 5 males. After non-fertile eggs were culled, embryos were exposed to vehicle (DMSO; 0.1%) or PCB-126 (50 nM) in filtered seawater (salinity 25 part per thousand, 65 embros per 20 ml in glass petri dish) for 4 hr at 20º C. After exposure, the embryos were washed in filtered seawater and incubated at 20º C under a 14-h light, 10-h dark cycle. At 5-, 10-, and 15-dpf, embryos were collected as three pools of 20 embryos from each treatment group and flash frozen in liquid nitrogen and stored at -80º C until used for RNA isolation. A loop design was used for the microarray hybridizations where each sample is hybridized to 2 arrays using both Cy3 and Cy5 labeled fluorophores. We used three loops in which each loop consisted of Cy3- and Cy5-labeled embryo aRNAs from 12 samples: one sample from each population-treatment-time combination. Within a population-treatment-time, embryos were randomly assigned to one of the three loops. In total, 36 embryos were hybridized to 36 microarrays. The loops formed were SC5C→ SC5P → NBH5C→ NBH5P →SC10C→ SC10P→ NBH10C→ NBH10P → SC15C→ SC15P → NBH15C → NBH15P → SC5C, where each arrow represents a separate hybridization (array) with the biological sample at the base of the arrow labeled with Cy3 and the biological sample at the head of the arrow labeled with Cy5. SC represents the Scorton Creek, Sandwich, MA population (reference), NBH represents the New Bedford Harbor, MA population, C represents control dose (DMSO), P represents the PCB-126 dose, 5 represents 5 dpf, 10 represents 10 dpf and 15 represents 15 dpf.
2011-06-06 | E-GEOD-25245 | biostudies-arrayexpress
Project description:Aluminum (Al) toxicity is a major factor limiting crop yields on acid soils. In maize, Al tolerance is a complex phenomenon involving multiple genes and physiological mechanisms yet uncharacterized. To begin elucidating the molecular basis of maize Al toxicity and tolerance, we performed a detailed temporal analysis of root gene expression under Al stress using microarrays with an Al-tolerant and an Al-sensitive maize genotype. Seedlings of both genotypes were grown in hydroponics in a full nutrient solution containing 39uM of free Al3+ activity. Root samples were collected at 'time zero', and after 2, 6 and 24 hours of treatment. Time course experiment with 0h, 2h, 6h and 24 hours of Al treatment in two maize genotypes contrasting for Al tolerance. The experimental design used for the microarray study was of two interconnected loops, and utilized a total of 16 slide sets. Samples collected from each genotype at one time point were contrasted with the previous and subsequent time points in a loop (4 time points x 2 genotypes = 8 slide sets). Additionally, the loops were interconnected (with dye swap) so that the two genotypes were contrasted directly at each time point (4 time points x 2 replicates = 8 slide sets). The design was balanced for dye distribution throughout samples and biological replicates. Each sample was labeled twice with Cy3 and twice with Cy5; each biological replicate had four samples labeled with Cy3 and four samples labeled with Cy5. The Sample signal intensity values were log2 transformed and analyzed by two interconnected ANOVA mixed models using PROC MIXED in SAS (Jin et al., 2001; Wolfinger et al., 2001). The normalization ANOVA model yij = µ + Ai + Dj + (A x D)ij + eij was applied to account for experiment-wide sources of variation associated with array (Ai, degrees of freedom (df) = 15, random effect), dye (Dj, df = 1, fixed effect), and their interactions. The residuals (eij) were treated as normalized values and analyzed in the following ANOVA model (gene model), where effects were evaluated for each gene individually: rikl = µ + Ai + Gk + Tl + (G x T)kl + ekl. Gk is the kth genotype (i.e. C100-6 or L53; df = 1) and represents the effect of each genotype on the expression of every gene, Tl represents the lth treatment (i.e. 0, 2, 6 or 24 hours of Al treatment; df = 3), and (G x T)kl the interaction between genotype and treatment (df = 3). Array (Ai) was included as a random effect to control for spot effects (Jin et al., 2001). Least square means were calculated, and estimates of differential expression were calculated as the difference between least-square means for each of the terms in the model. ANOVA results linked below as Supplementary files.
2010-05-26 | E-GEOD-10308 | biostudies-arrayexpress
Project description:Transcriptome profiling of tomato gene expression during fruit set
2009-05-06 | E-MEXP-1617 | biostudies-arrayexpress
Project description:Objective: To assess the role of aldoketoreductases and other doxorubicin pharmacokinetic or pharmacogenomic genes in doxorubicin cytotoxicity, resistance, DNA binding activity, and subcellular localization, Methods: We conducted a whole genome microarray study to identify differences in between doxorubicin-sensitive MCF-7cc cells and doxorubicin-resistant MCF-7Dox2-12 cells in terms of their expression of genes related to doxorubicin pharmacokinetics or pharmacodynamics. Targets were then validated by pharmacologic inhibition in conjunction with drug metabolite profiling, drug localization, drug cytotoxicity, and drug DNA binding studies. Results: 2063 differentially expressed transcripts were identified, including 17% and 43% of genes or gene families associated with doxorubicin pharmacokinetics or pharmacodynamics (p values of significance of 0.05 and <0.0001, respectively). The largest changes in the expression of genes associated with doxorubicin pharmacokinetics and pharmacodynamics were chiefly among the aldo-keto reductases (AKRs) Akr1c2, Akr1c3 and Akr1b10 which convert doxorubicin to doxorubicinol. We observed that doxorubicinol exhibits dramatically reduced drug toxicity, reduced drug DNA-binding activity, and altered drug subcellular localization to lysosomes. Pharmacologic inhibition of these AKRs in MCF-7Dox2-12 cells restored drug cytotoxicity, and drug localization to the nucleus. Conclusion: These findings demonstrate the utility of using curated pharmacokinetic and pharmacodynamic knowledgebases to identify highly relevant genes associated with doxorubicin resistance. The products of one or more of these genes could effectively be shown to alter the drug’s properties, while inhibiting them restored drug DNA binding, cytotoxicity, and subcellular localization. Doxorubicin resistant cell lines of breast MCF-7 cells were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with four labelling replicates of both forward and reverse labellings plus another set of 8 arrays with forward labelling. Sixteen arrays were used for this experiments. The co-cultured control cells MCF-7cc12 was generated by parallel selection process in the absence of drug.
2012-11-22 | E-GEOD-27254 | biostudies-arrayexpress
Project description:Background: Current protocols for the treatment of ovarian cancer include combination chemotherapy with a platinating agent and a taxane. However, many patients experience relapse of their cancer and the development of drug resistance is not uncommon, making successful second line therapy difficult to achieve. The objective of this study was to develop a cell line resistant to both carboplatin and docetaxel (dual drug resistant ovarian cell line A2780CBNDXL), along with single agent resistant lines (docetaxel resistant A2780DXL and carboplatin resistant A2780CBN), to investigate the mechanisms which underlie the development of dual drug resistance. Methods: The A2780 epithelial ovarian cancer cell line was used to select for isogenic carboplatin, docetaxel and dual drug resistant cell lines. A selection method of gradually increasing drug doses was implemented to avoid clonal selection. Resistance was confirmed using a clonogenic assay. Changes in gene expression associated with the development of drug resistance were determined by microarray analysis compared to parental co-culture control A2780CC. Changes in selected genes were validated by QPCR and immunoblotting. Results: Three isogenic cell lines were developed and resistance to each drug or the combination of drugs was confirmed. Development of resistance was accompanied by a reduced growth rate. The microarray and QPCR analyses showed that unique changes in gene expression occurred in the dual drug resistant cell line and that genes known to be involved in resistance could be identified in all cell lines. Conclusions: Novel changes in gene expression can occur in the development of dual drug resistance, indicating that dual drug resistance is not a simple combination of the changes occurring in single agent resistance Carboplatin, docetaxel (GSE26129) and carboplatin/docetaxel dual resistant cell lines of ovarian A2780 were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with two replicate of both forward and reverse labellings for each cell line. Four arrays were used for this experiments. And it was four replicate of both forward and reverse labellings for A2780 cells. Eight arrays were used for this experiments
2013-07-22 | E-GEOD-39337 | biostudies-arrayexpress
Project description:The taxanes are widely used in the treatment of breast and other cancers. While their cytotoxicity has been attributed to the induction of cell cycle arrest in mitosis through the stabilization of microtubules, we found that docetaxel promotes soluble tumor necrosis factor alpha (TNF-alpha production in MCF-7 breast tumor cells. TNF-alpha induces apoptotic cell death in a variety of cell types by binding to one of its receptors (TNFR1) which promotes death-inducing signaling complex (DISC) formation. Consistent with this view, we also report that selection of MCF-7 cells for survival in increasing concentrations of paclitaxel or docetaxel results in selection of drug-resistant variants that are resistant to TNF-alpha cytotoxicity. MCF-7 cells selected to 3-5 nM docetaxel produced >30-fold more TNF-alpha than control MCF-7CC cells but had strongly reduced levels of TNFR1. In contrast, expression of TNFR2 was unchanged, resulting in enhanced cell survival through the activation of the NF-kappaB p50 and p65 subunits. Gene expression profiling of docetaxel resistant MCF-7 cells compared to parental MCF-7 cells was performed for the changes of TNF related genes, and also confirmed in ovarian cell line A2780. Two docetaxel resistant cell lines of breast MCF-7 and ovarian A2780 were generated for gene expression profilling. Two colour microarray of Agilent whole human genome nucleotide arrays was conducted with two replicate of both forward and reverse labellings for MCF-7. Four arrays were used for this experiments. And it was four replicate of both forward and reverse labellings for A2780 cells. Eight arrays were used for this experiments
2011-12-30 | E-GEOD-26129 | biostudies-arrayexpress
Project description:Comparison of transcriptome and histone acetylation in Camponotus floridanus minor scout brains following 45 day treatment with small molecule pharmacologicals. The goal of this study was to characterize the molecular changes in gene expression and histone modification caused by ad lib feeding small molecule HAT and HDAC inhibitors Treated ants: 21 individual single brain samples, generating by linear amplification of polyA+ cDNA prepared from 15% of single brains; ChIP-seq for H3K9ac and H3K27ac was also prepared from 9 of these brains; ChIP-seq for H2O and C646 treated larvae also included; RNA-seq for technical replicate subsamples of a single brain also included
2015-12-10 | E-GEOD-69553 | biostudies-arrayexpress