Editor: Hyun Ah Kang
Differential glucose repression in common yeast strains in response to HXK2 deletion
Article first published online: 22 JAN 2010
© 2010 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved
FEMS Yeast Research
Volume 10, Issue 3, pages 322–332, May 2010
How to Cite
Kümmel, A., Ewald, J. C., Fendt, S.-M., Jol, S. J., Picotti, P., Aebersold, R., Sauer, U., Zamboni, N. and Heinemann, M. (2010), Differential glucose repression in common yeast strains in response to HXK2 deletion. FEMS Yeast Research, 10: 322–332. doi: 10.1111/j.1567-1364.2010.00609.x
Present address: Anne Kümmel, Novartis Institutes for BioMedical Research, Basel, Switzerland.
- Issue published online: 12 APR 2010
- Article first published online: 22 JAN 2010
- Received 17 July 2009; revised 4 January 2010; accepted 18 January 2010.Final version published online 24 March 2010.
- glucose repression;
- hexokinase 2;
Under aerobic, high glucose conditions, Saccharomyces cerevisiae exhibits glucose repression and thus a predominantly fermentative metabolism. Here, we show that two commonly used prototrophic representatives of the CEN.PK and S288C strain families respond differently to deletion of the hexokinase 2 (HXK2) – a key player in glucose repression: In CEN.PK, growth rate collapses and derepression occurs on the physiological level, while the S288C descendant FY4 Δhxk2 still grows like the parent strain and shows a fully repressed metabolism. A CEN.PK Δhxk2 strain with a repaired adenylate cyclase gene CYR1 maintains repression but not growth rate. A comparison of the parent strain's physiology, metabolome, and proteome revealed higher metabolic rates, identical biomass, and byproduct yields, suggesting a lower Snf1 activity and a higher protein kinase A (PKA) activity in CEN.PK. This study highlights the importance of the genetic background in the processes of glucose signaling and regulation, contributes novel evidence on the overlap between the classical glucose repression pathway and the cAMP/PKA signaling pathway, and might have the potential to resolve some of the conflicting findings existing in the field.