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.

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

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

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

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

Transmission of an entire human chromosome through the mouse male germline reveals an unexpectedly high tolerance of aneuploidy during male meiosis and results in accurate transcriptional deployment despite massive epigenetic remodeling during spermatogenesis.

The ribosomal protein, Rps27l, plays an oncogenic role by promoting p53 degradation via stabilizing the Mdm2-Mdm4 complex, but a tumor suppressor role by preventing the aneuploidy and loss of p53 heterozygosity.