Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA291873 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2144080.fastq.gz | Fastqsanger.gz | |||
| SRR2144081.fastq.gz | Fastqsanger.gz | |||
| SRR2144082.fastq.gz | Fastqsanger.gz | |||
| SRR2144083.fastq.gz | Fastqsanger.gz | |||
| SRR2144084.fastq.gz | Fastqsanger.gz |
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Project description:The involvement of protein chaperones in aging is intriguing and their potential contribution has, so far, been attributed solely to their central role in proteostasis. Here we show that four protein chaperones from different cellular compartments extend replicative lifespan (RLS) in budding yeast by a common mechanism akin to caloric restriction. The RLS extension relies on the increased direct activation of Snf1 kinase by Hsp90, thereby bypassing the signal on the environmental glucose level. The chaperone-related RLS extension is accompanied by the uncoupling of the respiratory chain. A genomic approach confirmed the repression of glycolysis and cytoplasmic translation, and contrary, activation of gluconeogenesis and fatty acid oxidation. Our results set a novel paradigm for the role of protein chaperones: by modulation of the chaperone expression level one can affect metabolic features such as glucose sensing, fatty acid consumption, respiration rate, and, consequently, modify lifespan. We expect the described mechanism to open new avenues for research in aging and age-related diseases.
2017-06-28 | GSE71711 | GEO
Project description:Sir2 is a highly conserved NAD+-dependent histone deacetylase that functions in heterochromatin formation and promotes replicative lifespan (RLS) in the budding yeast, Saccharomyces cerevisiae. Within the yeast rDNA locus, Sir2 is required for efficient cohesin recruitment and maintaining stability of the tandem array. In addition to the previously reported depletion of Sir2 in replicatively aged cells, we discovered that subunits of the Sir2 containing complexes, SIR and RENT, were depleted. Several other rDNA structural protein complexes also exhibited age-related depletion, most notably the cohesin complex. We hypothesized that mitotic chromosome instability (CIN) due to cohesin depletion could be a driver of replicative aging. ChIP assays of the residual cohesin (Mcd1-13xMyc) in moderately aged cells showed strong depletion from the rDNA and initial redistribution to the point centromeres, which was then lost in older cells. Despite the shift in cohesin distribution, sister chromatid cohesion was partially attenuated in aged cells and the frequency of chromosome loss was increased. This age-induced CIN was exacerbated in strains lacking Sir2 and its paralog, Hst1, but suppressed in strains that stabilize the rDNA array due to deletion of FOB1 or through caloric restriction (CR). Furthermore, ectopic expression of MCD1 from a doxycycline-inducible promoter was sufficient to suppress rDNA instability in aged cells and to extend RLS. Taken together we conclude that age-induced depletion of cohesin and multiple other nucleolar chromatin factors destabilize the rDNA locus, which then results in general CIN and aneuploidy that shortens RLS.
2019-03-12 | GSE117037 | GEO
Project description:Expression data from yeasts under non-caloric restriction (NR), caloric restriction (CR) and rapamycin treatment (RM)
| PRJNA324652 | ENA
Project description:Aneuploidy shortens replicative lifespan in Saccharomyces cerevisiae
| PRJNA305028 | 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: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. These are all CGH arrays comparing DNA content between the indicated strain of interest and a wt control.
2015-12-04 | E-GEOD-75623 | biostudies-arrayexpress
Project description:This study investigated the effects of TOR1 gene deletion on Saccharomyces cerevisiae through transcriptome analysis of wild-type and tor1Δ mutant cells during exponential development under non-stress circumstances. A significant number of differentially expressed genes (DEGs) were identified in the absence of TOR1, comprising 1665 upregulated genes and 1425 downregulated genes. These findings demonstrate the extensive impact of TOR signaling on several biological processes, including metabolism, stress response, and lifespan regulation. A significant number of differentially expressed genes (DEGs) were identified in the absence of TOR1, comprising 1665 upregulated genes and 1425 downregulated genes. These findings demonstrate the extensive impact of TOR signaling on several biological processes, including metabolism, stress response, and lifespan regulation. A total of 736 DEGs were associated with either replicative lifespan or chronological lifespan, further emphasizing the significance of TOR1 in aging. Although genes associated with glucose transporters and storage were upregulated, glycolytic genes remained unchanged, indicating a metabolic shift towards alternative pathways such as gluconeogenesis and the pentose phosphate pathway. Among these, HXK1 exhibited the highest upregulation in tor1Δ cells, contrasting with HXK2, whose expression remained stable. This suggests that HXK1, typically active under low glucose or caloric restriction, plays a crucial role in reregulating glucose metabolism in the absence of TOR1. The research also identified specific transcription factors, including ADR1, HAP4, and their paralogs, which were upregulated and bound only to the HXK1 promoter, pointing to their regulatory role in this metabolic shift. The findings indicate that TOR1 inactivation triggers nutrient- and energy-sensing mechanisms that redirect cellular resources towards stress adaptation and longevity, highlighting Tor1's crucial function in aging and proposing that modulation of the TOR pathway could be a potential strategy for anti-aging therapies.
2025-10-01 | GSE280426 | GEO
Project description:Caloric restriction extends lifespan and healthspan across species, with feeding times synchronized to circadian rhythms further maximizing its benefits. However, the mechanisms linking diet, diurnal rhythms, and lifespan are not fully understood. In mice, the time point most strongly tied to dietary effects on lifespan coincides with the peak of glucocorticoid secretion (ZT12, lights-off). Caloric restriction raises circulating glucocorticoid hormone levels, but their functional relevance remains untested. We show that the glucocorticoid receptor (GR) is critical for the effects of caloric restriction. Hepatocyte-specific GR mutant mice fail to respond to caloric restriction indicating that increased glucocorticoid amplitudes support its benefits. Using multiomics techniques in murine liver, we find that nutrient deprivation elicits a nuclear switch from active STAT signaling to increased FOXO1 activity, enabling the GR to activate a unique diet-specific gene expression program. Taken together, our results suggest that glucocorticoid rhythms are crucial for caloric restriction-induced metabolic reprogramming.
2025-11-04 | GSE298149 | GEO
Project description:Caloric restriction extends lifespan and healthspan across species, with feeding times synchronized to circadian rhythms further maximizing its benefits. However, the mechanisms linking diet, diurnal rhythms, and lifespan are not fully understood. In mice, the time point most strongly tied to dietary effects on lifespan coincides with the peak of glucocorticoid secretion (ZT12, lights-off). Caloric restriction raises circulating glucocorticoid hormone levels, but their functional relevance remains untested. We show that the glucocorticoid receptor (GR) is critical for the effects of caloric restriction. Hepatocyte-specific GR mutant mice fail to respond to caloric restriction indicating that increased glucocorticoid amplitudes support its benefits. Using multiomics techniques in murine liver, we find that nutrient deprivation elicits a nuclear switch from active STAT signaling to increased FOXO1 activity, enabling the GR to activate a unique diet-specific gene expression program. Taken together, our results suggest that glucocorticoid rhythms are crucial for caloric restriction-induced metabolic reprogramming.
2025-11-04 | GSE248866 | GEO
Project description:CAN1 Arginine Permease Deficiency Extends Yeast Replicative Lifespan via Translational Activation of Stress Response Genes
| PRJNA336542 | ENA