Publication

Ploidy tug-of-war: Evolutionary and genetic environments influence the rate of ploidy drive in a human fungal pathogen

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Last modified
  • 05/14/2025
Type of Material
Authors
    Aleeza C. Gerstein, University of Minnesota Twin CitiesHeekyung Lim, University of Minnesota Twin CitiesJudith Berman, University of Minnesota Twin CitiesMeleah Hickman, Emory University
Language
  • English
Date
  • 2017-04-01
Publisher
  • Wiley & SSE
Publication Version
Copyright Statement
  • © 2017 The Author(s). Evolution © 2017 The Society for the Study of Evolution.
Final Published Version (URL)
Title of Journal or Parent Work
Volume
  • 71
Issue
  • 4
Start Page
  • 1025
End Page
  • 1038
Grant/Funding Information
  • ACG was supported by a postdoctoral fellowship from the National Sciences and Engineering Research Council of Canada and a Banting Postdoctoral Fellowship from the Canadian Institutes of Health Research.
  • This work was supported by R01AI0624273 grant and an ERC Advanced Award 340087/RAPLODAPT to JB.
Supplemental Material (URL)
Abstract
  • Variation in baseline ploidy is seen throughout the tree of life, yet the factors that determine why one ploidy level is maintained over another remain poorly understood. Experimental evolution studies using asexual fungal microbes with manipulated ploidy levels intriguingly reveals a propensity to return to the historical baseline ploidy, a phenomenon that we term “ploidy drive.” We evolved haploid, diploid, and polyploid strains of the human fungal pathogen Candida albicans under three different nutrient limitation environments to test whether these conditions, hypothesized to select for low ploidy levels, could counteract ploidy drive. Strains generally maintained or acquired smaller genome sizes (measured as total nuclear DNA through flow cytometry) in minimal medium and under phosphorus depletion compared to in a complete medium, while mostly maintained or acquired increased genome sizes under nitrogen depletion. Improvements in fitness often ran counter to changes in genome size; in a number of scenarios lines that maintained their original genome size often increased in fitness more than lines that converged toward diploidy (the baseline ploidy of C. albicans). Combined, this work demonstrates a role for both the environment and genotype in determination of the rate of ploidy drive, and highlights questions that remain about the force(s) that cause genome size variation.
Author Notes
  • Correspondence: Aleeza C. Gerstein, gerst035@umn,edu
Keywords
Research Categories
  • Biology, Cell
  • Biology, Microbiology
  • Health Sciences, Human Development
  • Biology, Genetics

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