SUL1 deficiency reduces PKA activity to increase replicative lifespan in yeast Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA1036266 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26686574_1.fastq.gz | Fastqsanger.gz | |||
| SRR26686574_2.fastq.gz | Fastqsanger.gz | |||
| SRR26686575_1.fastq.gz | Fastqsanger.gz | |||
| SRR26686575_2.fastq.gz | Fastqsanger.gz | |||
| SRR26686576_1.fastq.gz | Fastqsanger.gz |
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Project description:The process of sulfate uptake plays a crucial role in cellular metabolism and growth. SUL1, a plasma membrane transporter responsible for regulating the entry of extracellular sulfate in S. cerevisiae. Our previous work verified SUL1 as a fundamental gene involved in the regulation of lifespan. This study aimed to undertake a more comprehensive analysis of the role of SUL1 in regulating longevity. Our data showed that that sulfate transport is not required for the effect of SUL1 deletion on increased longevity. The SUL1 mutant demonstrates decreased functionality within the PKA signaling pathway, resulting in a variety of effects, such as increased stress-protective trehalose and glycogen, enhanced autophagy, elevated expression of stress response genes, and reduced expression of ribosomal genes. Concurrently, the observed increase in lifespan resulting from the deletion of SUL1 may be partially attributed to the stimulation of autophagy and MSN2-mediated transcriptional activity. The findings of this study provide additional evidence for the association between sulfate transporter and longevity, thereby identifying a novel potential intervention target for extending lifespan.
2025-05-31 | GSE296216 | GEO
Project description:The process of sulfate uptake plays a crucial role in cellular metabolism and growth. SUL1, a plasma membrane transporter responsible for regulating the entry of extracellular sulfate in S. cerevisiae. Our previous work verified SUL1 as a fundamental gene involved in the regulation of lifespan. This study aimed to undertake a more comprehensive analysis of the role of SUL1 in regulating longevity. Our data showed that that sulfate transport is not required for the effect of SUL1 deletion on increased longevity. The SUL1 mutant demonstrates decreased functionality within the PKA signaling pathway, resulting in a variety of effects, such as increased stress-protective trehalose and glycogen, enhanced autophagy, elevated expression of stress response genes, and reduced expression of ribosomal genes. Concurrently, the observed increase in lifespan resulting from the deletion of SUL1 may be partially attributed to the stimulation of autophagy and MSN2-mediated transcriptional activity. The findings of this study provide additional evidence for the association between sulfate transporter and longevity, thereby identifying a novel potential intervention target for extending lifespan.
2023-11-09 | GSE247135 | GEO
Project description:SUL1 deficiency reduces PKA activity to increase replicative lifespan in yeast Saccharomyces cerevisiae
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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.
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Project description:Application of microfluidic platforms facilitated high-precision measurements of yeast replicative lifespan (RLS); however, comparative quantification of lifespan across strain libraries has been missing. Here we microfluidically measured RLS of 307 yeast strains, each deleted for a single gene. Despite previous reports of extended lifespan in these strains, we found that 56% of them did not actually live longer than the wild-type; while the remaining 44% showed extended lifespans, the degree of extension was often different from what was previously reported. Deletion of SIS2 gene led to the largest RLS increase observed. Sis2 regulated yeast lifespan in a dose-dependent manner, implying a role for the coenzyme A biosynthesis pathway in lifespan regulation. Introduction of the human PPCDC gene in the sis2Δ background neutralized the lifespan extension. RNA-seq experiments revealed transcriptional increases in cell-cycle machinery components in sis2Δ background. High-precision lifespan measurement will be essential to elucidate the gene network governing lifespan.
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Project description:In Saccharomyces cerevisiae, deletion of genes encoding proteins of the large ribosomal subunit (RPLs) increases the replicative lifespan in a Gcn4-dependent manner. However, how Gcn4, a key transcriptional activator of amino acid biosynthesis genes, increases lifespan, is unknown. Here we show that Gcn4 acts as a repressor of protein synthesis. By analyzing the mRNA and protein abundance, the ribosome occupancy and protein synthesis rate in various yeast strains, we demonstrate that Gcn4 is sufficient to reduce protein synthesis and to increase yeast lifespan. Chromatin immunoprecipitation reveals Gcn4 binding not only at genes that are activated, but also at genes that are repressed upon Gcn4 overexpression. The promoters of repressed genes contain Rap1 binding motifs. Our data suggest that Gcn4 is a central regulator of protein synthesis under multiple perturbations - including ribosomal protein (RP) gene deletions, calorie restriction, rapamycin treatment - and provide an explanation for its role in longevity and stress response. This SuperSeries is composed of the SubSeries listed below.
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Project description:In this study we perform ATAC-seq of budding yeast strains with variable copy number of the rRNA genes (rDNA CN). We aim to better understand the relationship between DNA accessibility and replicative lifespan in strains with variable rDNA CN.
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Project description:In Saccharomyces cerevisiae, deletion of genes encoding proteins of the large ribosomal subunit (RPLs) increases the replicative lifespan in a Gcn4-dependent manner. However, how Gcn4, a key transcriptional activator of amino acid biosynthesis genes, increases lifespan, is unknown. Here we show that Gcn4 acts as a repressor of protein synthesis. By analyzing the mRNA and protein abundance, the ribosome occupancy and protein synthesis rate in various yeast strains, we demonstrate that Gcn4 is sufficient to reduce protein synthesis and to increase yeast lifespan. Chromatin immunoprecipitation reveals Gcn4 binding not only at genes that are activated, but also at genes that are repressed upon Gcn4 overexpression. The promoters of repressed genes contain Rap1 binding motifs. Our data suggest that Gcn4 is a central regulator of protein synthesis under multiple perturbations - including ribosomal protein (RP) gene deletions, calorie restriction, rapamycin treatment - and provide an explanation for its role in longevity and stress response.
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Project description:In Saccharomyces cerevisiae, deletion of genes encoding proteins of the large ribosomal subunit (RPLs) increases the replicative lifespan in a Gcn4-dependent manner. However, how Gcn4, a key transcriptional activator of amino acid biosynthesis genes, increases lifespan, is unknown. Here we show that Gcn4 acts as a repressor of protein synthesis. By analyzing the mRNA and protein abundance, the ribosome occupancy and protein synthesis rate in various yeast strains, we demonstrate that Gcn4 is sufficient to reduce protein synthesis and to increase yeast lifespan. Chromatin immunoprecipitation reveals Gcn4 binding not only at genes that are activated, but also at genes that are repressed upon Gcn4 overexpression. The promoters of repressed genes contain Rap1 binding motifs. Our data suggest that Gcn4 is a central regulator of protein synthesis under multiple perturbations - including ribosomal protein (RP) gene deletions, calorie restriction, rapamycin treatment - and provide an explanation for its role in longevity and stress response.
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