A single gene allele underlies differences in aneuploidy tolerance in yeast.

Dosage-compensated gene expression facilitates chromosomal aneuploidy, which presents a rapid route to phenotypic evolution in natural yeast isolates.

Aneuploidy produces a protein expression signature characteristic of altered metabolism and redox homeostasis, and the loss of UBP6 ameliorates several aneuploidy-associated phenotypes.

Genetic analyses reveal that purely quantitative changes in the relative copy number of chromosomes can be sufficient to disrupt the epigenetic mechanisms that define the cells' differentiated state.

Many natural isolates of budding yeast carry extra chromosome copies and show lower-than-expected expression at a subset of amplified genes, which show unique evolutionary signatures.

Cell competition is an important mechanism selecting against aneuploid cells.

Detection of aneuploidy and/or mutations in ctDNA may represent a promising approach to detecting patients with MPNST.

RNA-level regulation of gene expression is negatively associated with protein-level regulation across cellular pathways in normal tissues and cancer.

Coordinated regulation of co-complex members compensates for aneuploidy-induced stoichiometric imbalances in human cancer.

The wtf meiotic drivers change the fitness landscape of meiosis in outcrossed Schizosaccharomyces pombe demonstrating that genetic parasites can favor the evolution of variants that disrupt meiotic fidelity.