Saccharomyces cerevisiae strain:BY4741/BY4742
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA601478 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11119550_1.fastq.gz | Fastqsanger.gz | |||
| SRR11119550_2.fastq.gz | Fastqsanger.gz | |||
| SRR11119551_1.fastq.gz | Fastqsanger.gz | |||
| SRR11119551_2.fastq.gz | Fastqsanger.gz | |||
| SRR11119552_1.fastq.gz | Fastqsanger.gz |
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Project description:Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.
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Project description:Epigenetic mechanisms including histone post-translational modifications control longevity in diverse organisms. Relatedly, loss of proper transcriptional regulation on a global scale is an emerging aspect of shortened lifespan, but the specific mechanisms linking these observations remain to be uncovered. Here, we describe a lifespan screen in S. cerevisiae, designed to identify altered amino acid residues of histones that alter yeast replicative aging. Our results reveal that lack of sustained H3K36 methylation is commensurate with increased cryptic transcription in a set of genes in old cells and shorter lifespan. Deletion of the K36me2/3 demethylase Rph1 increases H3K36me3 within these genes and suppresses cryptic transcript initiation to extend lifespan. We show that this aging phenomenon is conserved, as cryptic transcription also increases in old worms. We propose that epigenetic misregulation in aging cells leads to an increase in transcriptional noise that is detrimental to lifespan, and, importantly, this acceleration in aging can be reversed by restoring transcriptional fidelity.
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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:In the era of synthetic biology, design, construction, and utilization of synthetic chromosomes with unique features provide a new strategy to study complex cellular processes such as aging. Herein, we successfully constructed the 884 Kb synXIII of Saccharomyces cerevisiae to investigate replicative aging using this synthetic strains. We verified that up-regulation of a rRNA-related transcriptional factor, RRN9, positively influenced replicative lifespan. Using SCRaMbLE system that enables inducible whole-genome rearrangement on synXIII, we obtained 20 SCRaMbLEd synXIII strains with extended lifespan. Transcriptome analysis revealed the expression of genes involved in global protein synthesis is up-regulated in longer-lived strains. We established causal links between genotypic change and the long-lived phenotype via reconstruction of some key structural variations observed in post-SCRaMbLE strains and further demonstrated combinatorial effects of multiple aging regulators on lifespan extension. Our findings underscored the potential of synthetic yeasts in unveiling the function of aging-related genes.
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