Aneuploid proliferation defects in yeast are not driven by copy number changes of a few dosage-sensitive genes
Name
Bonney-2015-Aneuploid proliferat.pdf
Size
351.16 KB
Format
Adobe PDF
Checksum (MD5)
0647c5e4b4cf940114cfe93167668a2e
Author(s)
Moriya, Hisao
Bonney, Megan Ellis
Amon, Angelika B
Date Issued
May 2015
Journal
Genes & Development
Publisher
Cold Spring Harbor Laboratory Press
Citation
Bonney, Megan E., Hisao Moriya, and Angelika Amon. “Aneuploid Proliferation Defects in Yeast Are Not Driven by Copy Number Changes of a Few Dosage-Sensitive Genes.” Genes Dev. 29, no. 9 (May 1, 2015): 898–903.
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution-Noncommerical
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1101/gad.261743.115
