Aneuploid yeast strains show increased sensitivity to conditions that interfere with protein productionprotein synthesis and protein folding. This heightened sensitivity appears across multiple aneuploid strains carrying different extra chromosomes, indicating it is a general feature of aneuploidaneuploidy rather than dependent on which specific genes are duplicated. [@torres_effects_2007]
Definitions
- aneuploidaneuploidy
- protein productionprotein synthesis
- protein folding
- sensitivity
- euploid
- Aneuploid
Synthesis
Across multiple aneuploid yeast strains carrying different extra chromosomes, a consistent vulnerability to protein synthesis inhibitors emerges, establishing that this sensitivity is a general consequence of chromosome imbalance rather than specific gene dosage effects. The mechanistic basis for this heightened sensitivity appears to stem from proteotoxic stress caused by stoichiometric imbalances in cellular protein composition, as the additional protein production from extra chromosome genes disrupts the normal ratios of protein complexes and cellular machinery. This same imbalanced protein composition is proposed to drive other shared aneuploid phenotypes including cell cycle defects, proliferative disadvantage, and increased glucose uptake, all of which manifest regardless of which chromosome is duplicated. While the role of protein stoichiometry and proteotoxic burden is well-supported across these observations, the precise molecular mechanisms linking imbalanced protein composition to each specific phenotype, including the sensitivity to translation interference, remain incompletely resolved.
Related
- Aneuploidy impairs cell cycle progression in haploid yeast
- Extra chromosome genes drive aneuploid phenotypes through imbalanced protein composition
- Aneuploidy increases glucose uptake in yeast cells
- Aneuploidy causes proliferative disadvantage independent of extra chromosome identity