Aneuploid proliferation defects in yeast are not driven by copy number changes of a few dosage-sensitive genes

Megan E. Bonney, Hisao Moriya, Angelika Amon

Research output: Contribution to journalArticle

32 Citations (Scopus)

Abstract

Aneuploidy—the gain or loss of one or more whole chromosome— typically has an adverse impact on organismal fitness, manifest in conditions such as Down syndrome.A central question is whether aneuploid phenotypes are the consequence of copy number changes of a few especially harmful genes that may be present on the extra chromosome or are caused by copy number alterations of many genes that confer no observable phenotype when varied individually. We used the proliferation defect exhibited by budding yeast strains carrying single additional chromosomes (disomes) to distinguish between the “few critical genes” hypothesis and the “mass action of genes” hypothesis. Our results indicate that subtle changes in gene dosage across a chromosome can have significant phenotypic consequences. We conclude that phenotypic thresholds can be crossed by mass action of copy number changes that, on their own, are benign.

Original languageEnglish
Pages (from-to)898-903
Number of pages6
JournalGenes and Development
Volume29
Issue number9
DOIs
Publication statusPublished - May 1 2015

Keywords

  • Aneuploidy
  • Dosage-sensitive genes
  • Down syndrome
  • Proliferation

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology

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