Joanne Kingsbury, PhD

Cardenas – Lab Members

Joanne Kingsbury_Cardenas LabSenior Research Associate
317 CARL Building
Box 3054 DUMC
Durham, N.C. 27710
Phone: (919) 684-2809
Fax: (919) 684-2790

In 2000, I received my Ph.D. from the University of Canterbury, New Zealand, working with Jack Heinemann on a negative regulator of amino acid transport in the yeast Saccharomyces cerevisiae.

Following the completion of my doctoral studies, I joined John McCusker at Duke University Medical Center as a postdoctoral fellow, to investigate genetic requirements for fungal pathogenesis and in vivo survival, using clinically derived Saccharomyces cerevisiaeCandida albicans and Cryptococcus neoformans model systems. Specifically, I have determined that various fungal-specific amino acid biosynthetic enzymes are essential for fungal survival in vivo, and these provide an exciting, unexploited class of antifungal drug targets. Of particular interest are enzymes for which inhibition/mutation are fungicidal, as fungistatic inhibitors rely on a healthy immune system to clear existing fungi, while many infections occur in immunocompromised individuals.  Importantly, I have shown that components of the threonine biosynthetic pathway are essential for C. neoformans, and I have demonstrated the mechanisms behind the profoundly rapid and unprecedented serum sensitivity caused by mutation of certain threonine biosynthetic enzymes in both S. cerevisiae and C. albicans.

In 2010, I joined the Heitman group in collaboration with Sheldon Pinnell (Duke Department of Dermatology), to focus on novel strategies for the treatment of dermatophytic fungal infections.  Dermatophytic infections, such as those caused by Trichophyton species, are the most common cause of superficial mycoses worldwide, yet the limited range of therapeutic drugs available are fraught with problems such as high price, toxicity and/or poor efficacy.

In 2011, I transitioned to work with Maria Cardenas, investigating the regulation of the Target of Rapamycin Complex 1 (TORC1) pathway, again using a S. cerevisiae model system. TORC1 was first identified in yeast, and later shown to be highly conserved from yeast to humans, with clinical relevance in many areas such as fungal pathogenesis, ageing, transplant rejection, oncology, coronary artery restenosis and diabetes. Therefore, our research should fuel advances in understanding TORC1 signaling beyond the yeast model system.


Kingsbury, J. M., Sen, N. D., Maeda, T., Heitman, J. & Cardenas, M. E. 2014. Endolysosomal membrane trafficking complexes drive nutrient-dependent TORC1 signaling to control cell growth in Saccharomyces cerevisiae. Genetics 196, 1077-1089.

Gioti, A., Nystedt, B., Li, W., Xu, J., Andersson, A., Averette, A.F., Munch, K., Wang, X., Kappauf, C., Kingsbury, J.M., Kraak, B., Walker, L.A., Johansson, H.J., Holm, T., Lehtio, J., Stajich, J.E., Mieczkowski, P., Kahmann, R., Kennell, J.C., Cardenas, M.E., Lundeberg, J., Saunders, C.W., Boekhout, T., Dawson, T.L., Munro, C.A., de Groot, P.W., Butler, G., Heitman, J., Scheynius, A. 2013. Genomic insights into the atopic eczema-associated skin commensal yeast Malassezia sympodialis. mBio 4, e00572-00512.

Kingsbury, J. M., Heitman, J. & Pinnell, S. R. 2012. Calcofluor white combination antifungal treatments for Trichophyton rubrum and Candida albicans. PLoS One 7, e39405.

Kingsbury, J. M. & McCusker, J. H. 2010. Homoserine toxicity in Saccharomyces cerevisiae and Candida albicans homoserine kinase (thr1∆) mutants. Eukaryotic Cell 9, 717-728. *Featured as Eukaryotic Cell Article of Significant Interest and June 2010 Microbe Magazine Journal Highlights

Kingsbury, J. M. & McCusker, J. H. 2010. Fungal homoserine kinase (thr1∆) mutants are attenuated in virulence and die rapidly upon threonine starvation and serum incubation. Eukaryotic Cell 9, 729-737. * Featured as Eukaryotic Cell Article of Significant Interest and June 2010 Microbe Magazine Journal Highlights

Kingsbury, J. M. & McCusker, J. H. 2010. Cytocidal amino acid starvation of Saccharomyces cerevisiae and Candida albicans acetolactate synthase (ilv2∆) mutants is influenced by the carbon source and rapamycin. Microbiology 156, 929-939.

Kingsbury, J. M. & McCusker, J. H. 2008. Threonine biosynthetic genes are essential in Cryptococcus neoformansMicrobiology 154, 2767-2775.

Kingsbury, J. M., Goldstein, A. L., & McCusker, J. H. 2006. The role of nitrogen and carbon transport, regulation, and metabolism genes for Saccharomyces cerevisiae survival in vivoEukaryotic Cell 5, 816-824.

Pascon, R. C., Ganous, T. M., Kingsbury, J. M., Cox, G. M. & McCusker, J. H. 2004. Cryptococcus neoformans methionine synthase: expression analysis and requirement for virulence. Microbiology 150, 3013-3023.

Kingsbury, J. M., Yang, Z., Ganous, T. M., Cox, G. M. & McCusker, J. H. 2004. Novel chimeric spermidine synthase-saccharopine dehydrogenase gene (SPE3LYS9) in the human pathogen Cryptococcus neoformansEukaryotic Cell 3, 752-763.

Kingsbury, J. M., Yang, Z., Ganous, T. M., Cox, G. M. & McCusker, J. H. 2004. Cryptococcus neoformans Ilv2p confers resistance to sulfometuron methyl and is required for survival at 37˚C and in vivo. Microbiology 150, 1547-1558.