Wild type 4 hours exposure to congo red (cell wall chip)
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
SUBMITTER: Rosa Pérez-DÃaz
PROVIDER: E-GEOD-2106 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Data processing included: 1. Filtering of those bad quality image spots (these includes alterations on the shape or hybridization) 2. Filtering of low intensity which was done flagging with -50 those spots whose feature intensity was lower in any of both channels than the average of the local background in the corresponding channel for all spots. However, those genes whose feature intensity in one channel was under the limit but in the other channel was 5 times over limit were considered as on-off genes and were not filtered. 3. Filtering of low reproducibility intrachip replicated spots. Normal distribution was created with the value obtained from the formula: log2(Rax1/Rb) which means logarithm (two-based) of one ratio multiplied by the inverse of its replicate. This value for each gene shoud keep between the range of average ± 3SD. Those genes out of these range are flagged as -25 4. Normalization of ratios was done by Lowess mathematical method. Correction factor was 0.33 This SuperSeries is composed of the following subset Series: GSE960: wild type 0 hours exposure to congo red GSE961: wild type 2 hours exposure to congo red GSE962: wild type 4 hours exposure to congo red GSE963: wild type 6 hours exposure to congo red GSE964: slt2 mutant 4 hours exposure to congo red GSE965: rlm1 mutant 4 hours exposure to congo red GSE966: wild type two hours exposure to zymolyase Keywords: SuperSeries Refer to individual Series
2010-06-09 | E-GEOD-959 | biostudies-arrayexpress
Project description:Data processing included: 1. Filtering of those bad quality image spots (these includes alterations on the shape or hybridization) 2. Filtering of low intensity which was done flagging with -50 those spots whose feature intensity was lower in any of both channels than the average of the local background in the corresponding channel for all spots. However, those genes whose feature intensity in one channel was under the limit but in the other channel was 5 times over limit were considered as on-off genes and were not filtered. 3. Filtering of low reproducibility intrachip replicated spots. Normal distribution was created with the value obtained from the formula: log2(Rax1/Rb) which means logarithm (two-based) of one ratio multiplied by the inverse of its replicate. This value for each gene shoud keep between the range of average ± 3SD. Those genes out of these range are flagged as -25 4. Normalization of ratios was done by Lowess mathematical method. Correction factor was 0.33
2010-06-10 | E-GEOD-2105 | biostudies-arrayexpress
Project description:S. cerevisiae hog1 mutant strain was grown on YEPD. For Congo Red experiments, yest cells were grown overnight at 24 °C to an optical density 0.8 - 1 (A600). The culture was refreshed to 0.2 O.D and grown at 24 °C for 2h. Next, culture was divided into two parts. One continues growing under same conditions (non-treated culture) while the other was supplemented with Congo Red to a final concentration of 30 µg/ml. Cells were collected at 4hours of growth, frozen at -80 °C and processed for RNA extraction.
2010-06-10 | E-GEOD-2107 | biostudies-arrayexpress
Project description:S. cerevisiae was grown on YEPD. For yellow experiments, yeast cells were grown overnight at 24 °C to an optical density 0.8 - 1 (A600). The culture was refreshed to 0.2 O.D and grown at 24 °C for 6h. At this time cells were collected. Experiment was carried out hybridising the cDNA from the same RNA (from this culture) with both Cy3 and Cy5.
2010-06-10 | E-GEOD-2108 | biostudies-arrayexpress
Project description:Liver metastasis is one of the major causes of death in colorectal cancer (CRC) patients. To understand this process, we investigated whether the gene expression profiling of matched colorectal carcinomas and liver metastases could reveal key molecular events involved in tumor progression and metastasis. We performed experiments using a cDNA microarray containing 17,104 genes with the following tissue samples: paired tissues of 25 normal colorectal mucosa, 27 primary colorectal tumors, 13 normal liver and 27 liver metastasis, and 20 primary colorectal tumors without liver metastasis. To remove the effect of normal cell contamination, we selected 4,583 organ-specific genes with a false discovery rate (FDR) of 0.0067% by comparing normal colon and liver tissues using significant analysis of microarray, and these genes were excluded from further analysis. We then identified and validated 46 liver metastasis-specific genes with an accuracy of 83.3% by comparing the expression of paired primary colorectal tumors and liver metastases using prediction analysis of microarray. The 46 selected genes contained several known oncogenes and 2 ESTs. To confirm that the results correlated with the microarray expression patterns, we performed RT-PCR with WNT5A and carbonic anhydrase II. Additionally, we observed that 21 of the 46 genes were differentially expressed (FDR = 2.27%) in primary tumors with synchronous liver metastasis compared with primary tumors without liver metastasis. We scanned the human genome using a cDNA microarray and identified 46 genes that may play an important role in the progression of liver metastasis in CRC. Keywords: gene expression profiling using cDNA microarray We performed 17K cDNA microarray with the amplified RNAs from the following tissue samples: normal colorectal mucosa, primary colorectal tumors, normal liver and liver metastasis tumors, and primary colorectal tumors without liver metastasis. Organ-specific genes in normal colon and liver tissues were excluded from the pre-filtered genes, and then we discovered and validated liver metastasis-specific genes commonly up-regulated in the primary colorectal tumors and liver metastasis tumors. To confirm the microarray data, we performed a RT-PCR of two genes (WNT5A and carbonic anhydrase II) in the primary colorectal tumors with and without liver metastases.
2008-01-31 | E-GEOD-6988 | biostudies-arrayexpress
Project description:Primary productivity of open ocean environments, such as those inhabited by marine picocyanobacteria Synechococcus sp.WH8102, are often limited by low inorganic phosphate (P). To observe how this organism copes with P starvation, we constructed a full genome microarray and examined differences in gene expression under P-limited and P-replete growth conditions. To determine the temporal nature of the responses, comparisons were made for cells newly entered into P-stress (at a time point corresponding to the induction of extracellular alkaline phosphatase activity) and a later time point (late log phase). In almost all instances the P starvation response was transitory, with 36 genes showing significant upregulation (>log2 fold) while 23 genes were highly downregulated at the early time point; however, these changes in expression were maintained for only five of the upregulated genes. Knockout mutants were constructed for genes SYNW0947 or SYNW0948, comprising a two component regulator hypothesized to play a key role in regulating the response to P-limitation. A high degree of overlap in the sets of genes affected by P-limited conditions and in the knockout mutants supports this hypothesis; however there is some indication that other regulators may play a role in this response in Synechococcus sp. WH8102. Consistent with what has been observed in many other cyanobacteria, the Pho regulon of this strain is comprised largely of genes for alkaline phosphatases, P transport or P metabolism. Interestingly, however, the exact composition and arrangement of the Pho regulon appears highly variable in marine cyanobacteria. In this series four conditions have been analyzed. These are low phosphate stress during early log phase, low phosphate stress during late log phase, SYNW0947 mutation, and SYNW0948 mutation. There are six slides per condition, each with two biological replicates. There are three technical replicates for each biological replicate including one flip-dye comparison. The exception is the low phosphate stress during late log phase experiment which has a total of five slides, two biological replicates with three and two technical replicates, respectively, and one flip-dye comparison for each biological replicate. Each slide contains six replicate spots per gene.
2010-05-18 | E-GEOD-13170 | biostudies-arrayexpress
Project description:Marine cyanobacteria are thought to be the most sensitive of the phytoplankton groups to copper toxicity, yet little is known of the transcriptional response of marine Synechococcus to copper shock. Global transcriptional response to two levels of copper shock was assayed in both a coastal and an open ocean strain of marine Synechococcus using whole genome expression microarrays. Both strains showed an osmoregulatory-like response, perhaps as a result of increasing membrane permeability. This could have implications for marine carbon cycling if copper shock leads to dissolved organic carbon leakage in Synechococcus. The two strains additionally showed a reduction in photosynthetic gene transcripts. Contrastingly, the open ocean strain showed a typical stress response whereas the coastal strain exhibited a more specific oxidative or heavy metal type response. In addition, the coastal strain activated more regulatory elements and transporters, many of which are not conserved in other marine Synechococcus strains and may have been acquired by horizontal gene transfer. Thus, tolerance to copper shock in some marine Synechococcus may in part be a result of an increased ability to sense and respond in a more specialized manner. In this series four conditions have been analyzed. These are moderate copper shock for Synechococcus sp. WH8102 and CC9311 (pCu 11.1 and pCu 10.1, respectively), and high copper shock for WH8102 and CC9311 (pCu 10.1 and pCu 9.1, respectively). For each slide, an experimental RNA sample was labeled with Cy3 or Cy5 and was hybridized with a reference RNA from a non-copper-shocked sample labeled with the other Cy dye. There are six or eight slides per condition, each with two biological replicates. There are three or four technical replicates for each biological replicate including at least one flip-dye comparison. Each slide contains six replicate spots per gene.
2010-05-17 | E-GEOD-13910 | biostudies-arrayexpress
Project description:The GacS/GacA signal transduction system is a central regulator in Pseudomonas spp., including the biological control strain P. fluorescens Pf-5, in which GacS/GacA controls the production of secondary metabolites and exoenzymes that suppress plant pathogens. A whole genome oligonucleotide microarray was developed for Pf-5 and used to assess the global transcriptomic consequences of a gacA mutation in P. fluorescens Pf-5. In cultures at the transition from exponential to stationary growth phase, GacA significantly influenced transcript levels of 632 genes, representing more than 10% of the 6147 annotated genes in the Pf-5 genome. Transcripts of genes involved in the production of hydrogen cyanide, the antibiotic pyoluteorin, and the extracellular protease AprA were at a low level in the gacA mutant, whereas those functioning in siderophore production and other aspects of iron homeostasis were significantly higher in the gacA mutant than in wild-type Pf-5. Notable effects of gacA inactivation were also observed in the transcription of genes encoding components of a type VI secretion system and cytochrome C oxidase subunits. Two novel gene clusters expressed under the control of gacA were identified from transcriptome analysis, and we propose global-regulator-based genome mining as an approach to decipher the secondary metabolome of Pseudomonas spp. In this series two conditions have been analyzed. A gacA mutant of Pseudomonas fluorescens Pf-5 was harvested at early (OD 0.5) and late (OD 2.4) time points and compared to wild-type Pf-5 harvested in parallel. For each slide, an experimental RNA sample from a gacA mutant was labeled with Cy3 or Cy5 and was hybridized with a reference RNA sample from wild-type Pf-5 labeled with the other Cy dye. There are six slides per condition. Each condition is represented by three biological replicates. There are two flip-dye replicates for each biological replicate. Each slide contains three replicate spots per gene.
2010-03-03 | E-GEOD-16898 | biostudies-arrayexpress
Project description:A Saccharomyces cerevisiae population was cultured for many generations under conditions to which it is not optimally adapted. These experiments were designed to investigate adaptive evolution under natural selection. This study is described in more detail in Ferea TL, et al. 1999. Proc Natl Acad Sci USA 96:9721-6
2002-02-11 | E-GEOD-29 | biostudies-arrayexpress
Project description:Helicobacter pylori colonizes the stomach of half of the world's population, causing a wide spectrum of disease ranging from asymptomatic gastritis to ulcers to gastric cancer. Although the basis for these diverse clinical outcomes is not understood, more severe disease is associated with strains harboring a pathogenicity island. To characterize the genetic diversity of more and less virulent strains, we examined the genomic content of 15 H. pylori clinical isolates by using a whole genome H. pylori DNA microarray. We found that a full 22% of H. pylori genes are dispensable in one or more strains, thus defining a minimal functional core of 1281 H. pylori genes. While the core genes encode most metabolic and cellular processes, the strain-specific genes include genes unique to H. pylori, restriction modification genes, transposases, and genes encoding cell surface proteins, which may aid the bacteria under specific circumstances during their long-term infection of genetically diverse hosts. We observed distinct patterns of the strain-specific gene distribution along the chromosome, which may result from different mechanisms of gene acquisition and loss. Among the strain-specific genes, we have found a class of candidate virulence genes identified by their coinheritance with the pathogenicity island.
2001-07-25 | E-GEOD-6 | biostudies-arrayexpress