Send to

Choose Destination
PLoS Genet. 2017 May 24;13(5):e1006766. doi: 10.1371/journal.pgen.1006766. eCollection 2017 May.

Polymorphisms in the yeast galactose sensor underlie a natural continuum of nutrient-decision phenotypes.

Author information

Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, United States of America.
Department of Systems Biology, Harvard Medical School, Boston, Massachusetts, United States of America.
Systems Biology Graduate Program, Harvard University, Cambridge, Massachusetts, United States of America.
Ginkgo Bioworks, Boston, Massachusetts, United States of America.
Plant Systems Biology, School of Life Sciences Weihenstephan, Technische Universität, München, Freising, Germany.
Immuneering Corporation, Cambridge, Massachusetts, United States of America.


In nature, microbes often need to "decide" which of several available nutrients to utilize, a choice that depends on a cell's inherent preference and external nutrient levels. While natural environments can have mixtures of different nutrients, phenotypic variation in microbes' decisions of which nutrient to utilize is poorly studied. Here, we quantified differences in the concentration of glucose and galactose required to induce galactose-responsive (GAL) genes across 36 wild S. cerevisiae strains. Using bulk segregant analysis, we found that a locus containing the galactose sensor GAL3 was associated with differences in GAL signaling in eight different crosses. Using allele replacements, we confirmed that GAL3 is the major driver of GAL induction variation, and that GAL3 allelic variation alone can explain as much as 90% of the variation in GAL induction in a cross. The GAL3 variants we found modulate the diauxic lag, a selectable trait. These results suggest that ecological constraints on the galactose pathway may have led to variation in a single protein, allowing cells to quantitatively tune their response to nutrient changes in the environment.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center