Abstract

All proliferating cells need to match metabolism, growth and cell cycle progression with nutrient availability to guarantee cell viability in spite of a changing environment. In yeast, a signaling pathway centered on the effector kinase Snf1 is required to adapt to nutrient limitation and to utilize alternative carbon sources, such as sucrose and ethanol. Snf1 shares evolutionary conserved functions with the AMP-activated Kinase (AMPK) in higher eukaryotes which, activated by energy depletion, stimulates catabolic processes and, at the same time, inhibits anabolism. Although the yeast Snf1 is best known for its role in responding to a number of stress factors, in addition to glucose limitation, new unconventional roles of Snf1 have recently emerged, even in glucose repressing and unstressed conditions. Here, we review and integrate available data on conventional and non-conventional functions of Snf1 to better understand the complexity of cellular physiology which controls energy homeostasis.

Highlights

  • Cell growth and proliferation require a high amount of energy for biosynthetic pathways

  • Sip1 alone is not able to sustain growth on ethanol or glycerol and determines a very low kinase activity of the complex [13], Sip2 function seems to be involved in the mechanism of cellular aging [14], while Gal83 plays its main role in the Snf1-dependent transcriptional regulation, since in low glucose it determines the nuclear localization of the Snf1 complex thank to its NLS (Nuclear Localization Signal)

  • PERSPECTIVES AND CONCLUDING REMARKS Many studies have reported that AMPK activity is altered in several diseases, such as inflammation, diabetes and cancer [145, 146]

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Summary

Introduction

Cell growth and proliferation require a high amount of energy for biosynthetic pathways. Sip1 alone is not able to sustain growth on ethanol or glycerol and determines a very low kinase activity of the complex [13], Sip2 function seems to be involved in the mechanism of cellular aging [14], while Gal83 plays its main role in the Snf1-dependent transcriptional regulation, since in low glucose it determines the nuclear localization of the Snf1 complex thank to its NLS (Nuclear Localization Signal).

Results
Conclusion
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