Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA239807 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Chronological Aging of Yeast in the Absence of Caloric Restriction: Cell Immobilization Uncouples Reproduction from Metabolism
| PRJNA126547 | ENA
Project description:Aneuploidy and aging are correlated; however, a causal link between these two phenomena has remained elusive. Here we show that yeast disomic for a single native yeast chromosome generally have a decreased replicative lifespan. In addition, the extent of this lifespan deficit correlates with the size of the extra chromosome. We identified a mutation in BUL1 that rescues both the lifespan deficit and a protein trafficking defect in yeast disomic for chromosome 5. Bul1 is an E4 ubiquitin ligase adaptor involved in a protein quality-control pathway that targets membrane proteins for endocytosis and destruction in the lysosomal vacuole thereby maintaining protein homeostasis. Concurrent suppression of the aging and trafficking phenotypes suggests that disrupted membrane protein homeostasis in aneuploid yeast may contribute to their accelerated aging. The data reported here demonstrate that aneuploidy can impair protein homeostasis, shorten lifespan, and may contribute to age-associated phenotypes.
2015-12-04 | GSE75623 | GEO
Project description:Iron is an essential cofactor for enzymes involved in numerous cellular processes. We analyzed the metabolomes and transcriptomes of yeast grown in iron-rich and iron-poor media to determine which biosynthetic processes are altered when iron availability falls. Saccharomyces cerevisiae DBY7286 strain was grown from very low density to mid-log phase (A600 = 0.5, approximately 18 hrs.) in defined-iron SD minimal medium containing only the supplements necessary to meet auxotrophic requirements. Defined-iron SD minimal media were prepared with yeast nitrogen base lacking iron and copper, supplemented with 1 µM copper sulfate, 25 mM MES pH 6.1, 1 mM Ferrozine (Fluka), and the indicated concentrations of ferrous ammonium sulfate 10 µM (low iron) or 300 µM (high iron). All cells were grown at 30°C with shaking and four independent cultures were prepared for each growth condition
2009-11-12 | E-GEOD-19016 | biostudies-arrayexpress
Project description:Sit4 is a PP2A-like Ser/Thr protein phosphatase implicated in the regulation of cellular processes important for cell survival during aging. We have previously shown that SIT4 deletion promotes vacuolar acidification, mitochondrial derepression and oxidative stress resistance, increasing yeast chronological lifespan. In this study, we performed a proteomic analysis of isolated vacuoles and yeast genetic interaction analysis to unravel how Sit4 influences vacuolar and mitochondrial function. By employing high-resolution mass spectrometry, we show that sit4Δ vacuolar membranes were enriched in Vps27 and Hse1, two proteins that are part of the endosomal sorting complex required for transport-0 complex. In addition, SIT4 exhibited a negative genetic interaction with VSP27, as sit4∆vps27∆ double mutants had a shortened lifespan compared to sit4∆ and vps27∆ single mutants. Our results also show that Vps27 did not increase sit4∆ lifespan by improving protein trafficking or vacuolar sorting pathways. However, Vps27 was critical for iron homeostasis and mitochondrial function in sit4∆ cells, as sit4∆vps27∆ double mutants exhibited high iron levels, impaired mitochondrial respiration and mitochondrial DNA (mtDNA) depletion. These findings show for the first-time a cross-talk between Sit4 and Vps27, providing new insights into the mechanisms governing chronological lifespan.
2024-05-24 | PXD048450 | Pride
Project description:Yeast replicative aging is a process resembling replicative aging in mammalian cells. During aging, wild type haploid yeast cells enlarge, become sterile, and undergo nucleolar enlargement and fragmentation; we sought gene expression changes during the time of these phenotypic changes. Gene expression studied via microarrays and qPCR has shown reproducible, statistically significant changes in mRNA of genes at 12 and 18-20 generations. Our findings support previously described changes towards aerobic metabolism, decreased ribosome gene expression, and a partial Environmental Stress Response. Our novel findings include a pseudo-stationary phase, down-regulation of methylation-related metabolism, increased Nucleotide Excision Repair related mRNA, and a strong up-regulation of many of the regulatory subunits of protein phosphatase I (Glc7). These findings are correlated with aging changes in higher organisms as well as with the known involvement of protein phosphorylation states during yeast aging. J Gerontol, Jan, 2008, vol 63A, no. 1. Keywords: aging time course
2008-02-01 | GSE10018 | GEO
Project description:Expression time course of yeast grown in a minimal medium
| PRJNA244536 | ENA
Project description:Investigation of whole genome gene expression changes at short (2 hours) and extended (24 hours) timepoints in wild-type Saccharomyces cerevisiae treated with 50 μM menadione during exponential growth compared to an rph1Δ strain Transient treatment with 50 μM menadione elevates mitochondrial ROS and extends chronological lifespan in yeast. Deletion of RPH1, a H3K36me3 histone demethylase, block chronological lifespan extension. This study aimed to identify Rph1p-dependent gene expression changes induced by menadione treatment that may support chronological lifespan extension. Reference: Bonawitz, N.D., Chatenay-Lapointe, M., Wearn, C.M., and Shadel, G.S. (2008). Expression of the rDNA-encoded mitochondrial protein Tar1p is stringently controlled and responds differentially to mitochondrial respiratory demand and dysfunction. Curr Genet 54, 83-94.
2013-03-22 | GSE45383 | GEO