Editor: Martin Kupiec
The essence of yeast quiescence
Article first published online: 14 JUL 2011
© 2011 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Microbiology Reviews
Volume 36, Issue 2, pages 306–339, March 2012
How to Cite
De Virgilio, C. (2012), The essence of yeast quiescence. FEMS Microbiology Reviews, 36: 306–339. doi: 10.1111/j.1574-6976.2011.00287.x
- Issue published online: 8 FEB 2012
- Article first published online: 14 JUL 2011
- Accepted manuscript online: 9 JUN 2011 10:30AM EST
- Received 28 February 2011; accepted 19 May 2011.
- nutrient-signaling pathways;
- target of rapamycin complex 1 (TORC1);
- protein kinase A (PKA)
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.