Among ~5,000,000 fungal species on this planet, Candida albicans is unique in its lifelong association with humans, either as a stable component of the gastrointestinal microbiome or as the most common fungal pathogen. We hypothesize that this close relationship with the host has driven the evolution of specialized fungal programs for occupying a diversity of host niches. The core research objective of our laboratory is to define the molecular basis of host-microbe interactions that foster both commensalism and pathogenesis.
To approach these questions, we exploit genetic resources, animal models of virulence and commensalism, and techniques such as whole-genome chromatin immunoprecipitation and high throughput sequencing. To date we have identified a series of novel virulence factors that act independently of the yeast-to-hyphal transition, which was previously thought to be this species’ major virulence specialization (Noble et al., Nature Genetics 2010). Our detailed characterization of the Sef1 virulence factor uncovered a C. albicans-specific transcriptional network whose activity has opposite roles in commensalism and disseminated infections (Chen et al., Cell Host and Microbe 2011; Chen and Noble, PLoS Pathogens 2012).
More recently, we discovered that passage of C. albicans through the mammalian gastrointestinal milieu triggers a developmental switch to a commensalism-specific cell type (Pande et al., Nature Genetics 2013). The ability to switch between specialized cell types that are optimized for specific host niches helps to explain the ubiquity and versatility of this microorganism and offers opportunities for treatment and prevention of clinical infectious diseases.
Our laboratory is located on the 4th floor of Health Sciences East on the UCSF Parnassus campus. Our proximity to multiple laboratories focused on microbial pathogenesis and host defense promotes an exciting, interactive research environment. We are interested in recruiting outstanding students and postdoctoral fellows who wish to study host-pathogen interactions using cutting edge approaches. Contact information for Professor Noble: Suzanne.Noble[at]ucsf.edu.
Noble SM (2013). "Candida albicans specializations for iron homeostasis: from commensalism to virulence." Current Opinion in Microbiology 16(6): 708-715.
Pande K, Chen C, and Noble SM (2012). “Passage through the mammalian gut triggers a phenotypic switch that promotes Candida albicans commensalism.” Nature Genetics 45(9): 1088-91.
Chen C and Noble SM (2012). “Post-Transcriptional Regulation of the Sef1 Transcription Factor Controls the Virulence of Candida albicans in its Mammalian Host.” PLoS Pathogens 8(11): e1002956.
Chen C, Pande K, French SD, Tuch BB, and Noble SM (2011). “An Iron Homeostasis Regulatory Circuit With Reciprocal Roles in Candida albicans Virulence and Commensalism.” Cell Host and Microbe 10: 118-35.
Noble SM, French SD, Kohn LA, Chen V, and Johnson AD (2010). “Systematic Screens of a Candida albicans Homozygous Deletion Library Decouple Morphogenetic Switching and Pathogenicity.” Nature Genetics 42(7): 590-598.
Homann OR, Dea J, Noble SM, Johnson AD (2009). “A Phenotypic Profile of the Candida albicans Regulatory Network.” PLoS Genetics 5(12): e1000783.
Elson SL, Noble SM, Solis N, Filler SG, Johnson AD (2009). “An RNA Transport System in Candida albicans Regulates Hyphal Morphology and Invasive Growth.” PLoS Genetics 5(9): e1000664.
Liu OW, Chun CD, Chow,ED, Chen C, Madhani HD, Noble SM (2008). “Systematic Genetic Analysis of Virulence in the Human Fungal Pathogen Cryptococcus neoformans.” Cell 135: 174-88.
Noble, SM and Johnson, A (2007). "Genetics of Candida albicans, a Diploid Human Fungal Pathogen." Annual Review of Genetics 41: 193-211.
Noble SM and Johnson AD (2005). “Strains and Strategies for Large-Scale Gene Deletion Studies of the Diploid Human Fungal Pathogen, Candida albicans.” Eukaryotic Cell 4: 298-309.
Hromatka BS, Noble SM, Johnson AD (2005). “Transcriptional Response of C. albicans to Nitric Oxide and the Role of the YHB1 Gene in Nitrosative Stress and Virulence.” Molecular Biology of the Cell 16(10): 4814-26.