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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 ssd1\u0394 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.<\/jats:p>","DOI":"10.7554\/elife.52063","type":"journal-article","created":{"date-parts":[[2020,1,7]],"date-time":"2020-01-07T08:01:32Z","timestamp":1578384092000},"source":"Crossref","is-referenced-by-count":89,"title":["The genetic basis of aneuploidy tolerance in wild yeast"],"prefix":"10.7554","volume":"9","author":[{"given":"James","family":"Hose","sequence":"first","affiliation":[{"name":"Center for Genomic Science Innovation, University of Wisconsin\u2013Madison, Madison, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leah E","family":"Escalante","sequence":"additional","affiliation":[{"name":"Center for Genomic Science Innovation, University of Wisconsin\u2013Madison, Madison, United States"},{"name":"Laboratory of Genetics, University of Wisconsin-Madison, Madison, United 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