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Eukaryotic Cell, May 2006, p. 816-824, Vol. 5, No. 5
1535-9778/06/$08.00+0     doi:10.1128/EC.5.5.816-824.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Role of Nitrogen and Carbon Transport, Regulation, and Metabolism Genes for Saccharomyces cerevisiae Survival In Vivo{dagger}

Joanne M. Kingsbury, Alan L. Goldstein, and John H. McCusker*

Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710

Received 26 January 2006/ Accepted 7 March 2006

Saccharomyces cerevisiae is both an emerging opportunistic pathogen and a close relative of pathogenic Candida species. To better understand the ecology of fungal infection, we investigated the importance of pathways involved in uptake, metabolism, and biosynthesis of nitrogen and carbon compounds for survival of a clinical S. cerevisiae strain in a murine host. Potential nitrogen sources in vivo include ammonium, urea, and amino acids, while potential carbon sources include glucose, lactate, pyruvate, and fatty acids. Using mutants unable to either transport or utilize these compounds, we demonstrated that no individual nitrogen source was essential, while glucose was the most significant primary carbon source for yeast survival in vivo. Hydrolysis of the storage carbohydrate glycogen made a slight contribution for in vivo survival compared with a substantial requirement for trehalose hydrolysis. The ability to sense and respond to low glucose concentrations was also important for survival. In contrast, there was little or no requirement in vivo in this assay for any of the nitrogen-sensing pathways, nitrogen catabolite repression, the ammonium- or amino acid-sensing pathways, or general control. By using auxotrophic mutants, we found that some nitrogenous compounds (polyamines, methionine, and lysine) can be acquired from the host, while others (threonine, aromatic amino acids, isoleucine, and valine) must be synthesized by the pathogen. Our studies provide insights into the yeast-host environment interaction and identify potential antifungal drug targets.

* Corresponding author. Mailing address: Department of Molecular Genetics and Microbiology, Box 3020, Duke University Medical Center, Durham, NC 27710. Phone: (919) 681-6744. Fax: (919) 684-8735. E-mail: mccus001{at}mc.duke.edu.

{dagger} Supplemental material for this article may be found at http://ec.asm.org/.

Eukaryotic Cell, May 2006, p. 816-824, Vol. 5, No. 5
1535-9778/06/$08.00+0     doi:10.1128/EC.5.5.816-824.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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