Expression data of yeast genes treated with rapamycin and compound CID 3528206
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae Schizosaccharomyces pombe
PROVIDER: GSE33320 | GEO | 2012/05/01
SECONDARY ACCESSION(S): PRJNA149293
REPOSITORIES: GEO
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Project description:Compound CID 3538206 inhibits yeast TORC1 activity and functionally mimic rapamycin. We used microarrays to compare the global gene expression with the treatment of CID 3528206 and rapamycin. BY4741 yeast cells were treated with1% DMSO, 20 uM CID 3528206 and 200 nM rapamycin in duplicate for 3hrs. RNA extracted and labeled to probe yeast gene arrays
2012-04-30 | E-GEOD-33320 | biostudies-arrayexpress
Project description:This microarray data is the Affymetrix array of RNA expressed by Wild Type and Mutant strains yeast that is untreated and treated with rapamycin. In yeast, rapamycin inhibits the TORC1 kinase signaling pathway causing rapid alteration in gene expression and ultimately cell cycle arrest in G1 and this study provides a new insight whereby rapamycin signaling via the Torc1 kinase may exploit the pheromone pathway.
2022-04-25 | GSE201413 | GEO
Project description:Target of rapamycin complex 1 (TORC1) is implicated in growth control and aging from yeast to humans. Fission yeast is emerging as a popular model organism to study TOR signaling, although rapamycin has been thought to not affect cell growth in this organism. Here we analyzed the effects of rapamycin and caffeine, singly and combined, on multiple cellular processes in fission yeast. The two drugs led to diverse and specific phenotypes that depended on TORC1 signaling pathway inhibition, including prolonged chronological lifespan, inhibition of global translation, inhibition of cell growth and division, and reprogramming of global gene expression mimicking nitrogen starvation. Rapamycin and caffeine differentially affected these various TORC1-dependent processes. Combined drug treatment augmented most phenotypes and effectively blocked cell growth. Although rapamycin showed a much more subtle effect on global translation than did caffeine, rapamycin was more effective in prolonging chronological lifespan. Rapamycin prolonged the lifespan of non-growing cells only when applied during the growth phase but not when applied after cells had stopped proliferation. The doses of rapamycin and caffeine strongly correlated with growth inhibition and with lifespan extension. This comprehensive analysis will inform future studies into TORC1 function and cellular aging in fission yeast and beyond.
2013-05-05 | E-MTAB-1489 | biostudies-arrayexpress
Project description:CID 70698683 is a novel broad-spectrum antiviral compound. To understand the broad-spectrum antiviral mechanism, the cellular gene expression changes by the treatment of CID70698683 was measured.
2015-11-25 | GSE72167 | GEO
Project description:CID 70698683 is a novel broad-spectrum antiviral compound. To understand the broad-spectrum antiviral mechanism, the cellular gene expression changes by the treatment of CID70698683 was measured. HEp-2 cells grown in 6-well plates were treated with 5 microM of CID 70698683 for overnight and the cellular RNA was extracted (Treatment group). For control, DMSO was used instead of CID 70698683 (final concentration of 0.25%). Three replicates per group used.
2015-11-25 | E-GEOD-72167 | biostudies-arrayexpress
Project description:Target of Rapamycin Complex 1 (TORC1) signaling promotes growth and ageing. Inhibition of TORC1 leads to a down-regulation of factors that stimulate protein translation, which in turn contributes to longevity. TORC1-dependent post-transcriptional regulation of protein translation has been well studied, while analogous transcriptional regulation is less understood. Here we screened fission yeast deletion mutants for resistance to Torin1, which inhibits TORC1 and cell growth. Cells lacking the GATA transcription factor Gaf1 (gaf1Δ) grew normally even in high doses of Torin1. The gaf1Δ mutation shortened the chronological lifespan of non-dividing cells and diminished the longevity triggered by Torin1 treatment. Expression profiling and genome-wide binding experiments showed that, upon TORC1 inhibition, Gaf1 directly up-regulated genes for small-molecule metabolic pathways and indirectly repressed genes for protein translation. Surprisingly, Gaf1 bound to, and down-regulated the tRNA genes, so also functions as a transcription factor for genes transcribed by RNA polymerase III. Thus, Gaf1 controls the transcription of both coding and tRNA genes to inhibit translation and growth downstream of TORC1.
2020-03-02 | E-MTAB-8569 | biostudies-arrayexpress
Project description:To resolve the temporal sequence of phosphorylation events responding to nutritional and chemically induced up and downshifts of TORC1 signaling in S. cerevisiae wildtype, we performed quantitative MS phosphoproteomics upon nitrogen-quality up and downshifts and rapamycin treatment. We generated a high quality dataset byapplying a high resolution sampling, parallel sample processing and a dedicated data analysis pipeline that allowed us to select significant transient dynamics. By exploiting the temporal resolution of our data and the complementary of the shift experiments, we identified early phosphorylation changes regulated directly by TORC1 or by its proximal substrate kinases, and found both established and novel candidate TORC1 targets. Among the candidateTORC1 targets were the metabolic enzymes Amd1, Hom3, Nth1 and Tsl1, involved in nucleotide, amino acid and storage carbohydrate metabolism. Functional assessment of the role of phosphorylation for these and other enzymes was achieved by correlating phosphopeptide with the corresponding enzyme-associated metabolite dynamics. Candidate kinases regulating these enzymes were identified by establishing TORC1-proximity and differential kinase activity criteria. Our work provides first evidence of TORC1-dependent regulation of the metabolic enzymes Amd1and Hom3 by the kinases Sch9 and Atg1, respectively, providing mechanistic insights into on how TORC1 controls nucleotide and amino acid metabolism in response to the quality of the nitrogen source.
2022-02-22 | PXD000940 | Pride
Project description:Purpose:To identify the targets of TORC1 during spore germination in budding yeast Results:We obtained the transcriptomes of germinating spores in the presence and absence of rapamycin with and average Read Count = 14,009,863 and an Average Overall alignment: 95.23%. Differentialy expressed genes were identified by comparing the spore germination at various time points in the presence and absence of Rapamycin. Conclusions: Our transcriptomic analyses has revealed a role for TORC1 in regulating the glucose response genes
2019-12-31 | GSE110326 | GEO
Project description:The centromere-specific Histone H3-variant CENH3 (also known as CENP-A) is considered to be an epigenetic mark for establishment and propagation of centromere identity. Pulse-induction of CENH3 (Drosophila CID) in Schneider S2 cells incorporates into noncentromeric regions and generates CID islands that resist clearing from chromosome arms for multiple cell generations. We demonstrate that CID islands represent functional ectopic kinetochores, which are non-randomly distributed on the chromosome and display a preferential localization near telomeres and pericentric heterochromatin in transcriptionally silent, intergenic chromatin domains. Although overexpression of heterochromatin protein 1 (HP1) or increasing Histone acetylation interferes with CID islands formation on a global scale, induction of a locally defined region of synthetic heterochromatin by targeting HP1-LacI fusions to stably integrated Lac Operator arrays produces a proximal hotspot for CID islands formation. These data suggest that the characteristics of regions bordering heterochromatin promote de novo kinetochore assembly and thereby contribute to centromere identity. ArrayExpress Release Date: 2011-07-15 Person Roles: submitter Person Last Name: Diehl Person First Name: Sarah Person Mid Initials: Person Email: diehl@immunbio.mpg.de Person Phone: (+49) 761 5108 795 Person Address: Stuebeweg 51, 79108 Freiburg im Breisgau, Germany Person Affiliation: Max-Planck-Institute for Immunobiology and Epigenetics Person Roles: investigator Person Last Name: Heun Person First Name: Patrick Person Mid Initials: Person Email: heun@immunbio.mpg.de Person Phone: (+49) 761 5108 717 Person Address: Stuebeweg 51, 79108 Freiburg im Breisgau, Germany Person Affiliation: Max-Planck-Institute for Immunobiology and Epigenetics Publication Title: Heterochromatin boundaries are hotspots for de novo kinetochore formation. Publication Author List: Agata Olszak, Dominic van Essen, Antonio J. Pereira, Sarah Diehl, Thomas Manke, Helder Maiato, Simona Saccani and Patrick Heun
2012-01-20 | GSE30997 | GEO