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

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

Aneuploidy can cause chromosome mis-segregation and specific cellular phenotypes driven by expression of genes on the extra chromosome.

Cell competition is an important mechanism selecting against aneuploid cells.

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.

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

Strengthening of spindle assembly checkpoint activity and attachment error correction through BubR1 manipulation preserves genomic integrity and protects against tumor formation.

Chromosomal instability through spindle assembly checkpoint alleviation facilitates malignant transformation of hepatocytes and T-cells in vivo, resulting in cancers with recurrent karyotypes.

Multiple age-related changes in chromosome architecture could explain why human oocyte aneuploidy increases with advanced maternal age.