Aneuploid yeast strains bearing extra copies of different chromosomes all exhibit a proliferative disadvantage, meaning they grow more slowly or with reduced fitness compared to euploid strains. This disadvantage occurs regardless of which specific chromosome is duplicated, indicating that aneuploidaneuploidy itself—rather than the particular genes on extra chromosomes—is responsible for the growth impairment. [@torres_effects_2007]
Definitions
Synthesis
Across multiple studies in yeast systems, aneuploidy consistently causes a proliferative disadvantage regardless of which specific chromosome is duplicated, establishing that chromosome imbalance itself rather than the identity of extra genes drives this phenotype. The mechanistic basis for this general effect appears to be proteotoxic stress arising from stoichiometric imbalances in protein composition, as aneuploid strains uniformly show cell cycle delays, increased glucose uptake, and heightened sensitivity to protein synthesis interference independent of which chromosome is gained. These observations support the model that extra chromosome genes produce excess proteins that overwhelm cellular protein homeostasis systems, creating a universal burden that reduces fitness at both cellular and organismal levels. While the proteotoxic stress model provides a unifying explanation for the chromosome-independent proliferative disadvantage, the precise molecular mechanisms by which imbalanced protein stoichiometry translates into specific phenotypes like altered glucose metabolism remain an area requiring further investigation.
Related
- Aneuploidy impairs cell cycle progression in haploid yeast
- Extra chromosome genes drive aneuploid phenotypes through imbalanced protein composition
- Aneuploidy heightens sensitivity to protein synthesis interference
- Aneuploidy increases glucose uptake in yeast cells
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- Aneuploidy decreases both organismal and cellular fitness