Expression data from ETO2/LMO2 knockdown G1E-ER-GATA-1 cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Tohru Fujiwara
PROVIDER: E-GEOD-24359 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:We used microarrays to examine what genes could be regulated by ETO2 in erythroid cells. Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and ETO2(Cbfa2t3) siRNA on Agilent array. After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.
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Project description:We used microarrays to examine what genes could be regurated by LMO2 in erythroid cells. Comparing expression profile in murine G1E-ER-GATA-1 cells treated with control and Lmo2 siRNA on Agilent array. After siRNA transfection, the cells were treated with b-estradiol for 24h to induce GATA-1-mediated erythroid maturation.
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2008-03-28 | E-MEXP-1062 | biostudies-arrayexpress
Project description:These results were obtained in a controlled longitudinal experiment in which a group of rhesus macaques were exposed to a low dose of Mtb to study their progression to latent infection or active disease. Subsets of the animals were euthanized at scheduled time points, and granulomas taken from their lungs were assayed for gene expression. The clinical profiles associated with the animals following Mtb exposure revealed considerable variability, and we developed models for the disease trajectory for each subject using a Bayesian hierarchical B-spline approach. Disease severity estimates were derived from these fitted curves and included as covariates in linear models to identify genes significantly associated with disease progression. Our results demonstrate that the incorporation of clinical data increases the value of information extracted from the expression profiles and contributes to the identification of predictive biomarkers for TB susceptibility. Samples from 21 animals were included in this study. 18 rhesus macaques were exposed to Mtb and euthanisized according to a pre-defined schedule, and at least two granulomas were extracted from their lungs during necropsy. The remaining three animals were healthy controls and samples represent control lung tissues. The samples were arrayed using an extended loop design with animals grouped according to similar clinical profiles. Biological replication is provided in the form of at least two granuloma samples per animal.
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Project description:We proposed that DNA recombination/repair processes play a role in memory formation. Here, we used microarray analysis of rat amygdala genes to identify possible DNA recombination/repair factors involved in memory consolidation of conditioned taste aversion (CTA). Among the genes that showed statistically significant differential expression, we identified fen-1, encoding a flap-structure specific DNA endonuclease. Amygdalar fen-1 mRNA induction was associated to the illness component of CTA, since it could be observed by the pairing of a flavor and gastrointestinal illness, by the illness itself, but not by the presentation of the flavor alone. No CTA related induction of fen-1 expression was observed in the insular cortex. Importantly, functional validation studies demonstrated that amygdalar suppression of fen-1 expression impaired memory consolidation of CTA. Overall, our studies helped identify a new DNA recombination/repair candidate factor involved in memory formation of aversive experiences. Two comparisons were established between the cRNA samples: CTA versus Flavor-only and CTA versus Toxin-only. For each comparison, the microarray experiment was repeated four times using new biological samples, each consisting of a sample pool from 3 animals. Two of the four biological replicates were performed as dye-swaps in order to correct for dye bias effects.
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Project description:NIPP1 and EZH2 contribute to the silencing of a common set of genes. Since both NIPP1 and EZH2 turned out to be essential for the initiation and maintenance of global H3K27 trimethylation, a key step in the PcG-mediated transcriptional regulation of genes, we have subsequently examined by DNA-microarray analyses whether the loss of NIPP1 or EZH2 results in the expected regulation of a common set of genes. <br> <br> PC-3 cells were transfected in four independent experiments with a control siRNA or siRNA duplexes for the knockdown of EZH2 or NIPP1. To minimize indirect effects, RNA was already isolated 48h after transfection. At this time, the knockdown of NIPP1 or EZH2 was verified by quantitative qRT-PCR and amounted to 73 ± 7% and 82 ± 3% (n = 4), respectively. The isolated RNA pools were labeled with a fluorescent dye and were hybridized onto whole human genome Agilent gene chips. These chips contained 44,000 60-mer oligonucleotides, corresponding to ca 27,000 unambiguously annotated genes. Using SAM (significance analysis of microarray) analysis (P < 0.05), performed by comparing the NIPP1 or EZH2 knockdown against RNAi control, we selected 1581 and 2024 genes as significant in the NIPP1 or EZH2 knockdown, respectively. Using p<0.01, the loss of NIPP1 or EZH2 resulted in a significant upregulation of 281 genes and 319 genes, respectively, and downregulation of 409 and 175 genes respectively ). The knockdown of NIPP1 or EZH2 was confirmed in the microarray and the results of the expression array data were confirmed by qRT-PCR on a selection of affected genes, representing the entire range of fold-changes and using samples independent of those used for the microarray analysis.<br> <br> Strikingly, the list of the 50 genes that were most upregulated (SAM test, p<0.01) by the knockdown of NIPP1 were, in most cases, also upregulated following the knockdown of EZH2. In contrast, there was no obvious correlation between the 50 genes that were most downregulated after the knockdown of NIPP1 or EZH2. More detailed analysis revealed that 43% (121 genes) of the genes that were upregulated after the knockdown of NIPP1 were also upregulated by the loss of EZH2. In contrast, only 6% (25 genes) of the genes that were downregulated by the knockdown of NIPP1 were also downregulated by the loss of EZH2. Using another approach and using the list of significant genes based upon SAM test and p<0.05, we noted a significant linear correlation (R= 0.59 ± 0.01) between the extent to which genes were significantly upregulated by the loss of NIPP1 and the changes in the expression of these same genes following the knockdown of EZH2. No such correlation (R= 0.01 ± 0.01) was obtained for genes that were significantly downregulated. In the residual plot of these regressions, an obvious bend became apparent between the up and downregulated genes of the NIPP1 knockdown, confirming that we are in fact dealing with two differently regulated subpopulations. To validate this subdivision, the microarray data for a knockdown of EZH2, EED or SUZ12 which represent the core of the PRC2 complex, recently published by Bracken et al. ( 2006 ), were identically analyzed. In the residual plots, a bend between the up and downregulated genes was consistently present. We can conclude from our microarray data that NIPP1 silence a same set of genes as EZH2 and that NIPP1 also act as a transcriptional activator independent of EZH2.
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2012-12-16 | E-GEOD-42939 | biostudies-arrayexpress
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