Journal
FEMS MICROBIOLOGY REVIEWS
Volume 36, Issue 2, Pages 306-339Publisher
OXFORD UNIV PRESS
DOI: 10.1111/j.1574-6976.2011.00287.x
Keywords
quiescence; nutrient-signaling pathways; target of rapamycin complex 1 (TORC1); protein kinase A (PKA)
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Funding
- Swiss National Science Foundation
- Canton of Fribourg
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Like all microorganisms, yeast cells spend most of their natural lifetime in a reversible, quiescent state that is primarily induced by limitation for essential nutrients. Substantial progress has been made in defining the features of quiescent cells and the nutrient-signaling pathways that shape these features. A view that emerges from the wealth of new data is that yeast cells dynamically configure the quiescent state in response to nutritional challenges by using a set of key nutrient-signaling pathways, which (1) regulate pathway-specific effectors, (2) converge on a few regulatory nodes that bundle multiple inputs to communicate unified, graded responses, and (3) mutually modulate their competences to transmit signals. Here, I present an overview of our current understanding of the architecture of these pathways, focusing on how the corresponding core signaling protein kinases (i.e. PKA, TORC1, Snf1, and Pho85) are wired to ensure an adequate response to nutrient starvation, which enables cells to tide over decades, if not centuries, of famine.
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