Variation in the modality of a yeast signaling pathway is mediated by a single regulator

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Abstract

Bimodal gene expression by genetically identical cells is a pervasive feature of signaling networks, and has been suggested to allow organisms to hedge their "bets" in uncertain conditions. In the galactose-utilization (GAL) pathway of Saccharomyces cerevisiae, gene induction is unimodal or bimodal depending on natural genetic variation and pre-induction conditions. Here, we find that this variation in modality arises from regulation of two features of the pathway response: the fraction of cells that show induction, and their level of expression. GAL3, the galactose sensor, controls the fraction of induced cells, and titrating its expression is sufficient to control modality; moreover, all the observed differences in modality between different pre-induction conditions and amongst natural isolates can be explained by changes in GAL3's regulation and activity. The ability to switch modality by tuning the activity of a single protein may allow rapid adaptation of bet hedging to maximize fitness in complex environments.

Data availability

All data is deposited in a Dyrad repository (https://doi.org/10.5061/dryad.69p8cz8z8

The following data sets were generated

1. Springer M et al
(2021) Data from: Variation in the modality of a yeast signaling pathway is mediated by a single regulator
Dryad Digital Repository, doi:10.5061/dryad.69p8cz8z8.

https://doi.org/10.5061/dryad.69p8cz8z8

Article and author information

Author details

Julius Palme

Harvard Medical School, Boston, United States

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0001-5897-1334
Jue Wang

Department of Chemical Engineering, University of Washington, Seattle, United States

Competing interests
The authors declare that no competing interests exist.
Michael Springer

Harvard Medical School, Boston, United States

For correspondence
michael_springer@hms.harvard.edu

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-3970-6380

Funding

National Science Foundation (MCB-1349248)

Jue Wang
Michael Springer

National Institutes of Health (GM120122)

Julius Palme
Michael Springer

National Science Foundation (DGE1144152)

Jue Wang

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.