Msn2/4 regulate expression of glycolytic enzymes and control transition from quiescence to growth
Abstract
Nutrient availability and stresses impact a cell's decision to enter a growth state or a quiescent state. Acetyl-CoA stimulates cell growth under nutrient-limiting conditions, but how cells generate acetyl-CoA under starvation stress is less understood. Here, we show that general stress response factors, Msn2 and Msn4, function as master transcriptional regulators of yeast glycolysis via directly binding and activating genes encoding glycolytic enzymes. Yeast cells lacking Msn2 and Msn4 exhibit prevalent repression of glycolysis genes and a significant delay of acetyl-CoA accumulation and reentry into growth from quiescence. Thus Msn2/4 exhibit a dual role in activating carbohydrate metabolism genes and stress response genes. These results suggest a possible mechanism by which starvation-induced stress response factors may prime quiescent cells to reenter growth through glycolysis when nutrients are limited.
Data availability
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DynaMO, a package identifying transcription factor binding sites in dynamical ChIPSeq/RNASeq datasets, identifies transcription factors driving yeast ultradian and mammalian circadian cyclesPublicly available at the NCBI Gene Expression Omnibus (accession no: GSE72263).
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A high-resolution view of transcription and chromatin states across distinct metabolic states in budding yeastPublicly available at the NCBI Gene Expression Omnibus (accession no: GSE52339).
Article and author information
Author details
Funding
National Institutes of Health (U54GM103520)
- Zheng Kuang
- Jef D Boeke
National Institutes of Health (R01HG006841)
- Zheng Kuang
- Hongkai Ji
National Institutes of Health (R01HG006282)
- Zheng Kuang
- Hongkai Ji
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2017, Kuang et al.
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.
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