Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA151875 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Fitness Consequences of Aneuploidy Are Driven by Condition-Dependent Gene Effects
| PRJNA280885 | ENA
Project description:Aneuploidy has a myriad of consequences for health and disease, yet models of aneuploidy toxicity are still widely debated. To distinguish the effects of specific genes from the generalized burden of chromosome amplification, we measured the effects of duplicating individual genes in euploid cells as well as in select aneuploids using a barcoded plasmid library. We analyzed the responses of cells with and without extra chromosomes, as well as those with and without RNA-binding protein Ssd1. Deletion of Ssd1 sensitizes cells to chromosome amplification, but the source of this vulnerability is not known. Results of this experiment were used to interrogate determinants of aneuploidy toxicity, test models of Ssd1 dependence, and identify vulnerabilities of sensitized (ssd1-) and wild-type aneuploids. We also used the fitness effects of gene duplication in euploid cells to model the cost associated with chromosome duplication.
2024-05-01 | GSE263221 | GEO
Project description:Identification of Aneuploidy-Tolerating Mutations
| PRJNA125127 | 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 shortens replicative lifespan in Saccharomyces cerevisiae
| PRJNA305028 | ENA
Project description:Aneuploidy and ethanol tolerance in Saccharomyces cerevisiae
| PRJNA493718 | ENA
Project description:Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.
2017-09-12 | GSE98282 | GEO
Project description:Aneuploidy and epigenetic alterations have long been associated with carcinogenesis, but it was unknown whether aneuploidy could disrupt the epigenetic states required for cellular differentiation. In this study, we found that ~3% of random aneuploid karyotypes in yeast disrupt the stable inheritance of silenced chromatin during cell proliferation. Karyotype analysis revealed that this phenotype was significantly correlated with gains of chromosomes III and X. Chromosome X disomy alone was sufficient to disrupt chromatin silencing and yeast mating-type identity as indicated by a lack of growth response to pheromone. The silencing defect was not limited to the cryptic mating type loci but was associated with global changes in histone modifications and chromatin localization of Sir2 histone deacetylase. The chromatin-silencing defect of disome X can be partially recapitulated by increasing the copy number of several genes on chromosome X. These results suggest that aneuploidy can directly cause epigenetic instability and disrupt cellular differentiation.
2017-09-12 | GSE98435 | GEO
Project description:Effects of aneuploidy on cellular physiology and cell division in haploid yeast.
| PRJNA100035 | ENA