The genetic basis of aneuploidy tolerance in wild yeast

doi:10.7554/eLife.52063

Title: The genetic basis of aneuploidy tolerance in wild yeast

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Abstract

Aneuploidy is highly detrimental during development yet common in cancers and pathogenic fungi – what gives rise to differences in aneuploidy tolerance remains unclear. We previously showed that wild isolates of Saccharomyces cerevisiae tolerate chromosome amplification while laboratory strains used as a model for aneuploid syndromes do not. Here, we mapped the genetic basis to Ssd1, an RNA-binding translational regulator that is functional in wild aneuploids but defective in laboratory strain W303. Loss of SSD1 recapitulates myriad aneuploidy signatures previously taken as eukaryotic responses. We show that aneuploidy tolerance is enabled via a role for Ssd1 in mitochondrial physiology, including binding and regulating nuclear-encoded mitochondrial mRNAs, coupled with a role in mitigating proteostasis stress. Recapitulating ssd1D defects with combinatorial drug treatment selectively blocked proliferation of wild-type aneuploids compared to euploids. Our work adds to elegant studies in the sensitized laboratory strain to present a mechanistic understanding of eukaryotic aneuploidy tolerance.

Authors:

Hose, James ^[1]; Escalante, Leah E. ^[1]; Clowers, Katie J. ^[2]; Dutcher, H. Auguste ^[1]; Robinson, DeElegant ^[1]; Bouriakov, Venera ^[1]; Coon, Joshua J. ^[1]; Shishkova, Evgenia ^[1];

^[1]

Center for Genomic Science Innovation, University of Wisconsin-Madison, Madison, United States
Laboratory of Genetics, University of Wisconsin-Madison, Madison, United States

Publication Date:: 2020-01-07

Sponsoring Org.:: USDOE

OSTI Identifier:: 1581463

Alternate Identifier(s):: OSTI ID: 1581464

Grant/Contract Number:: SC0018409

Resource Type:: Published Article

Journal Name:: eLife

Additional Journal Information:: Journal Name: eLife Journal Volume: 9; Journal ID: ISSN 2050-084X

Publisher:: eLife Sciences Publications, Ltd.

Country of Publication:: United States

Language:: English

Citation Formats


                    Hose, James, Escalante, Leah E., Clowers, Katie J., Dutcher, H. Auguste, Robinson, DeElegant, Bouriakov, Venera, Coon, Joshua J., Shishkova, Evgenia, and Gasch, Audrey P. The genetic basis of aneuploidy tolerance in wild yeast.  United States: N. p., 2020. 
        Web.  doi:10.7554/eLife.52063.

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                    Hose, James, Escalante, Leah E., Clowers, Katie J., Dutcher, H. Auguste, Robinson, DeElegant, Bouriakov, Venera, Coon, Joshua J., Shishkova, Evgenia, & Gasch, Audrey P. The genetic basis of aneuploidy tolerance in wild yeast.  United States.  doi:10.7554/eLife.52063.

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                    Hose, James, Escalante, Leah E., Clowers, Katie J., Dutcher, H. Auguste, Robinson, DeElegant, Bouriakov, Venera, Coon, Joshua J., Shishkova, Evgenia, and Gasch, Audrey P. Tue .  
        "The genetic basis of aneuploidy tolerance in wild yeast".  United States.  doi:10.7554/eLife.52063.

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@article{osti_1581463,

  title        = {The genetic basis of aneuploidy tolerance in wild yeast},

  author       = {Hose, James and Escalante, Leah E. and Clowers, Katie J. and Dutcher, H. Auguste and Robinson, DeElegant and Bouriakov, Venera and Coon, Joshua J. and Shishkova, Evgenia and Gasch, Audrey P.},

  abstractNote = {Aneuploidy is highly detrimental during development yet common in cancers and pathogenic fungi – what gives rise to differences in aneuploidy tolerance remains unclear. We previously showed that wild isolates of Saccharomyces cerevisiae tolerate chromosome amplification while laboratory strains used as a model for aneuploid syndromes do not. Here, we mapped the genetic basis to Ssd1, an RNA-binding translational regulator that is functional in wild aneuploids but defective in laboratory strain W303. Loss of SSD1 recapitulates myriad aneuploidy signatures previously taken as eukaryotic responses. We show that aneuploidy tolerance is enabled via a role for Ssd1 in mitochondrial physiology, including binding and regulating nuclear-encoded mitochondrial mRNAs, coupled with a role in mitigating proteostasis stress. Recapitulating ssd1D defects with combinatorial drug treatment selectively blocked proliferation of wild-type aneuploids compared to euploids. Our work adds to elegant studies in the sensitized laboratory strain to present a mechanistic understanding of eukaryotic aneuploidy tolerance.},

  doi          = {10.7554/eLife.52063},

  journal      = {eLife},

  number       = ,

  volume       = 9,

  place        = {United States},

  year         = {2020},

  month        = {1}

}

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