cell aging | SGD

Datasets 84 datasets for 56 references

Dataset	Description	Keywords	Number of Conditions	Reference
A cell non-autonomous mechanism of yeast chronological aging regulated by caloric restriction and one-carbon metabolism	Purpose: To gain additional insights to candidate factors promoting longevity in Caloric Restricted Conditioned Media (CRCM), we performed transcriptomics analysis (RNA-seq) on BY4741 yeast cells grown in non-restricted SC media supplemented with CRCM, Non-restricted Conditioned Media (NRCM), or water as a control with a goal of identifying physiological responses that could be linked to specific metabolites. Methods: RNA profiles of NR (SC, 2% glucose) treated cells supplemented with water, 2% CRCM, or 2% NRCM at log phase, 24, and 96 hours post-inoculation. These samples were conducted in triplicate. Following inoculation, we harvested cells at log phase, 24 hrs (late diauxic shift), and 96 hrs (stationary phase).Total RNA was isolated using the hot acid phenol method and then processed into Illumina DNA sequencing libraries. Briefly, total RNA was treated with DNase I for 10 min at 37°C and then measured for concentration and quality with an Agilent Bioanalyzer. PolyA mRNA selection was performed on 5µg of the DNase-treated total RNA with the NEBNext Poly(A) mRNA magnetic isolation module (E7490). DNA sequencing libraries were then generated with the NEBNExt Ultra Directional RNA library Prep kit for Illumina (E7420). Libraries were sequenced on an Illumina NextSeq 500 by the UVA Genome Analysis and Technology Core. Results: Sequencing reads were mapped to the sacCer3 genome using bowtie2 with default settings. We preprocessed sequencing data from the UVA genomics core and analyzed differential gene expression in R using DESeq2. We found that In log phase cells, there were no significantly upregulated or downregulated genes in the CRCM or NRCM samples as compared to the water supplemented control (FDR <0.05). At the 24 hr timepoint, CRCM samples diverged from the NRCM and water supplemented control samples, and showed many more differentially regulated genes than the NRCM-treated samples. At the 96 hr timepoint, NRCM samples also became more clearly separated from the control in a PCA plot , though there were still a large number of genes exclusively altered in the CRCM samples. Furthermore, the YCL064C (CHA1) gene clearly stood out as being the most significantly upregulated in conditioned media supplementation. Conclusions: RNAseq data led us to explore YCL064C (CHA1) gene clearly stood out as being the most significantly upregulated in the conditioned media experiments. CHA1 encodes a predominantly mitochondrial L-serine (L-threonine) deaminase that catabolizes these amino acids. RNA-seq based transcriptome analysis allowed us to explore L-serine contribution to longevity phenotype we observed with CRCM.	cell aging	27	Enriquez-Hesles E, et al. (2021) PMID:33243834
A prion accelerates proliferation at the expense of lifespan	Organisms often commit to one of two strategies: living fast and dying young or living slow and dying old. In fluctuating environments, however, switching between these two strategies could be advantageous. Lifespan is often inversely correlated with cell size and proliferation, which are both limited by protein synthesis. Here we report that a highly conserved RNA-modifying enzyme, the pseudouridine synthase Pus4/TruB, can act as a prion, endowing yeast with greater proliferation rates at the cost of a shortened lifespan. Cells harboring the prion can grow larger and exhibit altered protein synthesis. This epigenetic state, [BIG+] (better in growth), allows cells to heritably yet reversibly alter their translational program, leading to the differential expression of hundreds of proteins, including many that regulate proliferation and aging. Our data reveal a functional role for aggregation of RNA-modifying enzymes in driving heritable epigenetic states that transform cell growth and survival.	cell aging, prions	10
Ageing transcriptomes of selected mutants on different carbon sources	Here we show that an unrestricted galactose diet in early life minimises pathology during replicative ageing in budding yeast, irrespective of diet later in life. Lifespan and average mother cell division rate are comparable between glucose and galactose diets, but markers of senescence and the progressive dysregulation of gene expression observed on glucose are minimal on galactose, showing these to be facets of ageing pathology rather than intrinsic parts of the replicative ageing process. Respiration on galactose is critical for minimising ageing pathology, and forced respiration during ageing on glucose by over-expression of Hap4 also has the same effect though only in a fraction of cells. This fraction maintains Hap4 activity to advanced age with low senescence and a youthful gene expression profile, whereas other cells in the same population that lose Hap4 activity undergo dramatic dysregulation of gene expression and accumulate aneuploid fragments of chromosome XII aneuploidy (ChrXIIr), which are tightly associated with ageing pathology.	cell aging	118
Analysing the impact of extrachromosomal rDNA circles (ERCs) on the ageing yeast transcriptome	This SuperSeries is composed of the SubSeries listed below.	cell aging	60
Analysing the impact of extrachromosomal rDNA circles (ERCs) on the ageing yeast transcriptome [genome]	Here we analysed the widespread disruption of gene expression that accompanies yeast ageing, and surprisingly observed that this is completely independent of ERCs. Furthermore, we could not find subsets of genes that are differentially regulated in the presence of ERCs. High throughput imaging showed that the accumulation of Tom70-GFP which accompanies the onset of cell division defects at the Senescence Entry Point (SEP) also correlated poorly to ERC abundance, but allowed determination of a gene expression signature for the SEP. This signature included overexpression of mRNA from the chromosome XII region between the rDNA and the telomere (ChrXIIr), which has been previously noted to amplify during ageing.	cell aging	12
Analysing the impact of extrachromosomal rDNA circles (ERCs) on the ageing yeast transcriptome [RNA]	Here we analysed the widespread disruption of gene expression that accompanies yeast ageing, and surprisingly observed that this is completely independent of ERCs. Furthermore, we could not find subsets of genes that are differentially regulated in the presence of ERCs. High throughput imaging showed that the accumulation of Tom70-GFP which accompanies the onset of cell division defects at the Senescence Entry Point (SEP) also correlated poorly to ERC abundance, but allowed determination of a gene expression signature for the SEP. This signature included overexpression of mRNA from the chromosome XII region between the rDNA and the telomere (ChrXIIr), which has been previously noted to amplify during ageing.	cell aging	48
Analyzing the impact of extrachromosomal rDNA circles (ERCs) on the ageing yeast transcriptome	Here we analyzed the widespread disruption of gene expression that accompanies yeast ageing, and surprisingly observed that this is completely independent of ERCs. Furthermore, we could not find subsets of genes that are differentially regulated in the presence of ERCs. High throughput imaging showed that the accumulation of Tom70-GFP which accompanies the onset of cell division defects at the Senescence Entry Point (SEP) also correlated poorly to ERC abundance, but allowed determination of a gene expression signature for the SEP. This signature included overexpression of mRNA from the chromosome XII region between the rDNA and the telomere (ChrXIIr), which has been previously noted to amplify during ageing.	cell aging	24
Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [MoBYSeqData]	Premature aging is a hallmark of Down syndrome, caused by trisomy of human chromosome 21; but the reason is unclear and difficult to study in humans. We used an aneuploid model in wild yeast to show that chromosome amplification disrupts nutrient-induced cell-cycle arrest, quiescence entry, and healthy aging, across genetic backgrounds and amplified chromosomes. We discovered that these defects are due in part to aneuploidy-induced dysfunction in Ribosome Quality Control (RQC). Aneuploids entering quiescence display aberrant ribosome profiles, accumulate RQC intermediates, and harbor an increased load of protein aggregates. Although they have normal proteasome capacity, aneuploids show signs of ubiquitin dysregulation, which impacts cyclin abundance to disrupt arrest. Remarkably, inducing ribosome stalling in euploids produces similar aberrations, while up-regulating limiting RQC subunits or proteins in ubiquitin metabolism alleviates many of the aneuploid defects. Our results raise major implications for other aneuploidy disorders including Down syndrome.	ploidy, cell aging	18
Aneuploidy induces premature aging in yeast due to defects in Ribosome Quality Control [RNASeqData]	Premature aging is a hallmark of Down syndrome, caused by trisomy of human chromosome 21; but the reason is unclear and difficult to study in humans. We used an aneuploid model in wild yeast to show that chromosome amplification disrupts nutrient-induced cell-cycle arrest, quiescence entry, and healthy aging, across genetic backgrounds and amplified chromosomes. We discovered that these defects are due in part to aneuploidy-induced dysfunction in Ribosome Quality Control (RQC). Aneuploids entering quiescence display aberrant ribosome profiles, accumulate RQC intermediates, and harbor an increased load of protein aggregates. Although they have normal proteasome capacity, aneuploids show signs of ubiquitin dysregulation, which impacts cyclin abundance to disrupt arrest. Remarkably, inducing ribosome stalling in euploids produces similar aberrations, while up-regulating limiting RQC subunits or proteins in ubiquitin metabolism alleviates many of the aneuploid defects. Our results raise major implications for other aneuploidy disorders including Down syndrome.	ploidy, cell aging	40
Aneuploidy shortens replicative lifespan in Saccharomyces cerevisiae	Aneuploidy and aging are correlated; however, a causal link between these two phenomena has remained elusive	cell aging, ploidy	24	Sunshine AB, et al. (2016) PMID:26762766

Showing 1 to 10 of 84 entries

records per page

Download (.txt)

Analyze

Additional Keywords