A central goal of evolutionary genetics is to understand, at the molecular level, how organisms adapt to their environments. Landmark work has characterized steric clashes between variants arising in a given protein as it evolves a new function. For many traits, any such single gene represents only part of a complex architecture, whose genetic mechanisms remain poorly understood. We studied the joint effect of eight genes underlying thermotolerance in Saccharomyces cerevisiae, when introduced into a thermosensitive species, S. paradoxus. The data revealed no sign epistasis: most gene combinations boosted thermotolerance, and none was deleterious. And the genes also governed a heretofore unknown advantage in cold growth by S. paradoxus. These results shed light on how and why thermotolerance arose in S. cerevisiae, and they suggest a paradigm in which, if protein repacking is a difficult step in adaptation, combining whole-gene modules may be far less constrained.
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