Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA92621 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:S. cerevisiae mutant with a constitutively activated Ras/cAMP pathway
| PRJNA85397 | ENA
Project description:Nutrient-Regulated Antisense and Intragenic RNAs Modulate a Signal Transduction Pathway
| PRJNA109829 | ENA
Project description:Cells need to coordinate gene expression with their metabolic states to maintain cell homeostasis and growth. However, how cells transduce nutrient availability to appropriate gene expression response via histone modifications remains poorly understood. Here, we report that glycolysis promotes H3K4me3 by activating Tpk2, the catalytic subunit of protein kinase A (PKA) via the Ras-cyclic AMP (cAMP) pathway. Further study showed that Tpk2 antagonizes Jhd2-catalyzed H3K4 demethylation by phosphorylating Jhd2 at S321 and S340 in response to glucose availability.Mechanistically, Tpk2-catalyzed Jhd2 phosphorylation inhibits its overall binding to chromatin and promotes its polyubiquitination by the E3 ubiquitin ligase Not4 and degradation by the proteasome. In addition, Tpk2-catalyzed Jhd2 phosphorylation also maintains H3K14ac by preventing the binding of Rpd3 to chromatin. By inhibiting the activity of Jhd2 and Rpd3, Tpk2-catalyzed Jhd2 phosphorylation regulates gene expression and promotes autophagy. Thus, regulation of Jhd2 by the Ras-cAMP-PKA pathway shed lights on how cells rewire their biological responses to glucose availability.
2022-08-29 | GSE175868 | GEO
Project description:In this study, we used Saccharomyces cerevisiae to investigate the effects of GRX deletion on yeast chronological life span (CLS). Deletion of Grx1 or Grx2 shortened yeast CLS. Quantitative proteomics revealed that GRX deletion increased cellular ROS levels to activate Ras/PKA signal pathway. Our results provided new insights into mechanisms underlying aging process.
2022-02-25 | PXD009699 | Pride
Project description:Comparison of the transcriptomes of Saccharomyces cerevisiae wild type FY23 and a PDE2 deletion mutant DJ28. Keywords = PDE2 Keywords = Ras/cAMP pathway Keywords: other
2003-08-19 | GSE600 | GEO
Project description:Comparison of the transcriptomes of Saccharomyces cerevisiae wild type FY23 and a PDE2 deletion mutant DJ28. Keywords = PDE2 Keywords = Ras/cAMP pathway
2010-06-05 | E-GEOD-600 | biostudies-arrayexpress
Project description:Asc1p and its essential orthologues in higher eukaryotes, as e.g. RACK1 in mammals, are involved in several distinct cellular signaling processes, but the implications of a total deletion have never been assessed in a comprehensive genome-wide manner. This study reveals the major cellular processes affected in a Saccharomyces cerevisiae Δasc1 deletion background via de novo proteome and transcriptome analysis, as well as subsequent phenotypical characterizations. The deletion of ASC1 reduces iron-uptake and causes nitrosative stress, both known indicators for hypoxia, which manifests in a shift of energy metabolism from respiration to fermentation in the Δasc1 strain. The impact of Asc1p in cellular metabolism is further expressed by its regulative role in the MAP kinase signal transduction pathways of invasive/filamentous growth, pheromone response and cell wall integrity. In the Δasc1 mutant strain aberrations from the expected cellular response, mediated by these pathways, can be observed and are linked to changes in protein abundances of pathway-targeted transcription factors. Evidence for the translational regulation of such transcription factors suggests that ribosomal Asc1p is involved in signal transduction pathways by controlling the biosynthesis of the respective final transcriptional regulators.
2012-11-30 | GSE34286 | GEO
Project description:Expression data for filamentous-form yeast with genetic perturbations
| PRJNA97385 | ENA
Project description:Cotranslational signal independent SRP preloading during membrane targeting
| PRJNA300274 | ENA
Project description:Extracellular superoxide dismutase (SOD3), which dismutases hydrogen peroxide to superoxide anion at cell membranes, mimics RAS oncogene action inducing primary cell immortalization at sustained low-level expression while high expression activates cancer barrier signaling through p53-p21 growth arrest pathway. We have previously demonstrated that the growth regulation of SOD3 occurs at the level of RAS and is mediated through non-transcriptional and transcriptional routes. Therefore, in the current work we assayed the growth suppressive mechanisms of SOD3 by characterizing the main signal transduction routes from the cell membrane into the nucleus. Based on our data robust over-expression of SOD3 in anaplastic thyroid cancer 8505c cells increased EGFR, RYK, ALK, FLT3, and EPHA10 tyrosine kinase receptor phosphorylation with consequent downstream SRC, FYN, YES, HCK, and LYN kinase activation. However, RAS pull-down experiment suggested lack of mitogen pathway stimulation that was confirmed by MEK1/2 and ERK1/2 Western blot. Interestingly, mRNA expression analysis indicated that SOD3 regulated in a dose dependent manner the expression of selected guanine nucleotide exchange factors (Rho GEF16, Ral GEF RGL1), GTPase activating proteins (ArfGAP ADAP2, Ras GAP RASAL1, RGS4), and Rho guanine nucleotide disassociation inhibitors (Rho GDI 2) therefore controlling the signal transduction through RAS GTPases to downstream signal transduction pathways. Our current data suggests a SOD3-induced activation of growth signal transduction is controlled in a dose dependent manner through GEF, GAP, and GDI.
2014-12-31 | GSE56546 | GEO