Transcription profiling of yeast haploid and heterozygous essential deletion pools treated with compounds involved in copper metabolism
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ABSTRACT: The haploid and the heterozygous essential S.cerevisiae deletion pools were grown in the presence of compounds that cause copper metabolism phenotypes in zebrafish. These experimental samples were hybridized against DMSO control samples. The resulting hybridization pattern informs about sensitive and resistant yeast deletion mutants. This data is used to draw conclusions about potential target pathways of these compounds in the cell.
Project description:The haploid and the heterozygous essential S.cerevisiae deletion pools were grown in the presence of compounds that we found to be synergistic with fluconazole. We also treated the deletion pools with combinations of those drugs and fluconazole to interrogate the mechanism of action of the drug interactions. These experimental samples were hybridized against DMSO or water control samples. The resulting hybridization pattern informs about sensitive and resistant yeast deletion mutants.
Project description:This SuperSeries is composed of the following subset Series: GSE29606: Gene expression profiles of effector T cells induced by mTOR inhibition GSE29607: Comparison of gene expression profiles of effector T cells from leptin-receptor-deficient mice and wild type mice Refer to individual Series
Project description:The Meu5 RNA-binding protein stabilises its targets during meiosis. We used an in vivo labelling system (Cleary et al. 2005 Nat Biotechnol. 23, 232-7) to estimate the decay rates of meu5delta and wild type cells over-expressing the transcription factor Mei4.
Project description:The Meu5 RNA-binding protein stabilises its targets during meiosis. We compared wild type and meu5delta cells transcriptome under different conditions: pat1-induced meiosis in diploid cells, wild type meiosis in diploid cells and cells overexpressing the Mei4 transcription factor.
Project description:We have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed during leptin receptor deficiency, which is partly responsible for the inhibition of T cell effector functions. Mouse CD4+CD25- T cells were purified from leptin-receptor-deficient mice and wild type mice, and stimulated with anti-CD3 and anti-CD28 for 12h. Six mice of each genotype were used. Leptin receptor deficiency-induced gene expression profiles were evaluated in mouse effector T cells from db/db mice and compared to the ones observed in their WT counterpart (db/+ mice). Two independent experiments were performed, and in each of them, 3 mice/group were pooled.
Project description:To further develop our gene expression approach to treatment of autoimmunity, we have employed whole genome microarray expression profiling as a discovery platform to identify genes differentially expressed upon immunosuppressor treatment responsible for inhibition of T cell effector functions. Human CD4+CD25- cells from healthy donors were pretreated or not with rapamycin and stimulated with anti-CD3 and anti-CD28 for 12h. mTOR (Mammalian Target of Rapamycin) inhibition-induced gene expression was evaluated in human effector T cells after 1 hour rapamycin pretreatment and compared to vehicle-pretreated cells. Three independent experiments were performed for each of the two different experimental conditions using different donors for each experiment.
Project description:To find out possible pathways and processes influenced by DmMANF we compared the changes in MANF null and overexpressing animals. We used two developmental stages of Drosophila, st 17 embryos and 29-50 hrs after egg laying (AEL) larvae. The timing were decided according to the lethality of MANF mutants with or without maternal contribution of MANF. Maternal and zygotic MANF mutants (MANFmzD96) were compared to paternal rescue and wild type embryos of the same age. Zygotic MANF mutants (MANFD96) with maternal contribution were compared to wild type and MANF ectopic overexpression larvae harvested well before the average lethality occured (75 hrs AEL). The changes in expression profiles were more drastic in MANFmzD96 embryos than in MANFD96 larvae. Gene ontology annotations were analyzed and clustered by DAVID. The major result was alterations in membranes, changes in membrane transporter expressions and disturbed intracellular membrane traffic. The results were verified by qPCR and transmission electron microscopy. Two developmental stages - 21-24 hrs and 29-50 hrs AEL of MANFD96 mutants without and with maternal contribution were compared to wild type (Wmix means crossed w1118 x w- ) and with paternal rescue or ectopic overexpression of MANF respectively by Drosophila Agilent microarray expression platform.
Project description:The Meu5 RNA-binding protein stabilises its targets during meiosis. To investigate the function of Meu5 we induced synchronous meiosis in wild type or meu5delta cells (using pat1 thermo-sensitive mutations), and measured mRNA levels at regular intervals.
Project description:The presence of Set2-mediated methylation of H3K36 (K36me) correlates with transcription frequency throughout the yeast genome. K36me targets the Rpd3S complex to deacetylate transcribed regions and suppress cryptic transcription initiation at certain genes. Here, using a genome-wide approach, we report that the Set2-Rpd3S pathway is generally required for controlling acetylation at coding regions. When using acetylation as a functional read-out for this pathway, we discovered that longer genes and, surprisingly, genes transcribed at lower frequency exhibit a stronger dependency. Moreover, a systematic screen using high resolution tiling microarrays allowed us to identify a group of genes that rely on Set2-Rpd3S to suppress spurious transcripts. Interestingly, most of these genes are within the group that depend the same pathway to maintain a hypo-acetylated state at coding regions. These data highlight the importance of using the functional readout of histone codes to define the roles of specific pathways.