Expression profiling analyses for 5 maize inbreds and 4 hybrids, chosen to represent diversity in genotypes and heterosis responses, revealed a correlation between genetic diversity and transcriptional variation. The majority of differentially expressed genes in each of the different hybrids exhibited additive expression patterns, and ~25% exhibited statistically significant non-additive expression profiles. Among the non-additive profiles, ~80% exhibited hybrid expression levels between the parental levels, ~20% exhibited hybrid expression levels at the parental levels and ~1% exhibited hybrid levels outside the parental range. These findings indicate that the frequencies of additive and non-additive expression patterns are very similar across a range of hybrid lines.
Gene expression analyses in maize inbreds and hybrids with varying levels of heterosis.
No sample metadata fields
View SamplesExpression profiling analyses for eight maize inbreds reveals extensive transcriptional variation. Many genes exhibit presence-absence variation among the inbred lines.
Gene expression analyses in maize inbreds and hybrids with varying levels of heterosis.
No sample metadata fields
View SamplesTrancript Based Cloning (TBC) uses standard Gene Expression techniques to quickly isolate genes of interest and begin to determine their function. Using a particular mutant phenotype, identified during a programme of mutagenesis and screning, and a wild-type control we can quickly determine a list of genes that is likely to contain the gene responsible for the phenotype. TBC is a general method for identifying and cloning important plant genes that is fast and may be applicable to almost any plant species Transcript abundance assays on the barley rar1-2 mutant and Sultan5 wild type were performed by using standard methods for the Affymetrix barley genome array (Affymetrix). For each genotype, two independent biological replicates were analyzed and pooled for analysis. Data were analyzed with DCHIP VERSION 1.3 (www.dchip.org),using data from only perfect-match oligonucleotides. Model-based analysis was performed by using perfect match-only analysis, compiling data from two biological replicates for each condition. Pairwise comparisons were analyzed for each condition, and a lower 90% confidence bound (LCB) and fold change were determined for each comparison. Gene expression changes were considered significant if the LCB was 1.4-fold or higher and if the intensities between the two conditions differed by >100. ****[PLEXdb(http://www.plexdb.org) has submitted this series at GEO on behalf of the original contributor, james hadfield. The equivalent experiment is BB5 at PLEXdb.]
A Ca2+/calmodulin-dependent protein kinase required for symbiotic nodule development: Gene identification by transcript-based cloning.
Specimen part
View SamplesGenome-wide analysis of GBM-derived brain tumor stem cells-like (BTSCs) collected at the Freiburg Medical Center and UAB (JX6)
NF1 regulates mesenchymal glioblastoma plasticity and aggressiveness through the AP-1 transcription factor FOSL1.
Specimen part, Disease, Disease stage
View SamplesExpression data from HEK293 cells expressing a doxcycline-inducible RANBP6 shRNA
EGFR feedback-inhibition by Ran-binding protein 6 is disrupted in cancer.
Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Translational control of the oogenic program by components of OMA ribonucleoprotein particles in Caenorhabditis elegans.
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View SamplesThe oocytes of most animals arrest at diplotene or diakinesis, but resume meiosis (meiotic maturation) in response to hormones. In C. elegans, maturation of the 1 oocyte requires the presence of sperm, Gas-adenylate cyclase-PKA signaling in the gonadal sheath cells, and germline function of two Tis11-like CCCH zinc-finger proteins, OMA-1 and OMA-2 (OMA proteins). Prior studies indicate that the OMA proteins redundantly repress the translation of specific mRNAs in oocytes (zif-1, mom-2, nos-2, glp-1) and early embryos (mei-1).
Translational control of the oogenic program by components of OMA ribonucleoprotein particles in Caenorhabditis elegans.
No sample metadata fields
View SamplesThe oocytes of most animals arrest at diplotene or diakinesis, but resume meiosis (meiotic maturation) in response to hormones. In C. elegans, maturation of the –1 oocyte requires the presence of sperm, Gas-adenylate cyclase-PKA signaling in the gonadal sheath cells, and germline function of two Tis11-like CCCH zinc-finger proteins, OMA-1 and OMA-2 (OMA proteins). Prior studies indicate that the OMA proteins redundantly repress the translation of specific mRNAs in oocytes (zif-1, mom-2, nos-2, glp-1) and early embryos (mei-1). We purified OMA-1-containing ribonucleoprotein particles (RNPs) and identified mRNAs that associate with OMA-1 in oocytes using microarrays. We examined the relative abundances of mRNAs in OMA-1 RNPs using high-throughput RNA sequencing. Previously identified targets of OMA-dependent translational repression in oocytes were found to be both enriched (>2-fold relative to input RNA) and abundant in purified OMA-1 RNPs. Furthermore, we verified that some of the newly identified mRNAs that share these characteristics are translationally repressed by OMA-1/2 in oocytes through sequences in their 3’UTRs. Although meiotic maturation is stimulated by sperm, we found that the mRNAs copurifying with OMA-1 are not significantly different in the presence and absence of sperm, suggesting that sperm-dependent signaling does not modify the suite of mRNAs stably associated with OMA-1. Further, several tested OMA-1-associated mRNAs were shown to be translationally repressed in both the presence and absence of sperm. Overall design: C. elegans mRNAs that co-purify with OMA-1 were identified by deep-sequencing using the Illumina HiSeq 2000
Translational control of the oogenic program by components of OMA ribonucleoprotein particles in Caenorhabditis elegans.
Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
An inhibitor of mutant IDH1 delays growth and promotes differentiation of glioma cells.
Specimen part, Treatment
View SamplesThe recent discovery of mutations in metabolic enzymes has rekindled interest in harnessing the altered metabolism of cancer cells for cancer therapy. One potential drug target is isocitrate dehydrogenase 1 (IDH1) which is mutated in multiple human cancers. Here, we examine the role of mutant IDH1 in fully transformed cells with endogenous IDH1 mutations. A selective R132H-IDH1 inhibitor (AGI-5198) identified through a high-throughput screen dose-dependently blocked the ability of the mutant enzyme (mIDH1) to produce R-2-hydroxyglutarate (R-2HG). Under conditions of near complete R-2HG inhibition, the mIDH1 inhibitor induced demethylation of histone H3K9M3 and expression of genes associated with gliogenic differentiation. Blockade of mIDH1 impaired the growth of IDH1-mutant - but not IDH1-wildtype glioma cells without appreciable changes in genome wide DNA methylation. These data suggest that mIDH1 may promote glioma growth through mechanisms beyond its well-characterized epigenetic effects.
An inhibitor of mutant IDH1 delays growth and promotes differentiation of glioma cells.
Specimen part, Treatment
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