Polyploidy can drive rapid adaptation in yeast.

Nature
Authors
Keywords
Abstract

Polyploidy is observed across the tree of life, yet its influence on evolution remains incompletely understood. Polyploidy, usually whole-genome duplication, is proposed to alter the rate of evolutionary adaptation. This could occur through complex effects on the frequency or fitness of beneficial mutations. For example, in diverse cell types and organisms, immediately after a whole-genome duplication, newly formed polyploids missegregate chromosomes and undergo genetic instability. The instability following whole-genome duplications is thought to provide adaptive mutations in microorganisms and can promote tumorigenesis in mammalian cells. Polyploidy may also affect adaptation independently of beneficial mutations through ploidy-specific changes in cell physiology. Here we perform in vitro evolution experiments to test directly whether polyploidy can accelerate evolutionary adaptation. Compared with haploids and diploids, tetraploids undergo significantly faster adaptation. Mathematical modelling suggests that rapid adaptation of tetraploids is driven by higher rates of beneficial mutations with stronger fitness effects, which is supported by whole-genome sequencing and phenotypic analyses of evolved clones. Chromosome aneuploidy, concerted chromosome loss, and point mutations all provide large fitness gains. We identify several mutations whose beneficial effects are manifest specifically in the tetraploid strains. Together, these results provide direct quantitative evidence that in some environments polyploidy can accelerate evolutionary adaptation.

Year of Publication
2015
Journal
Nature
Volume
519
Issue
7543
Pages
349-52
Date Published
2015 Mar 19
ISSN
1476-4687
URL
DOI
10.1038/nature14187
PubMed ID
25731168
PubMed Central ID
PMC4497379
Links
Grant list
U54 CA143798 / CA / NCI NIH HHS / United States
R37 GM061345 / GM / NIGMS NIH HHS / United States
R37 GM61345 / GM / NIGMS NIH HHS / United States
Howard Hughes Medical Institute / United States
U54CA143798 / CA / NCI NIH HHS / United States
R01 GM081617 / GM / NIGMS NIH HHS / United States