Abstract

The yeast Candida albicans is a normal resident of the human digestive tract. It is also the most common fungal pathogen of humans, causing both mucosal and systemic infections, particularly in immune compromised patients. This proposal seeks to understand how C. albicans orchestrates its many interactions with the host. Our strategy is to approach aspects of commensalism and pathogenicity through dissection of the transcriptional circuitry that controls these processes. Our overarching goal is to understand how C. albicans is specialized to thrive and cause disease in many different environments of the host.

Public Health Relevance

C. albicans is the most prevalent fungal pathogen of humans. It causes superficial infections in normal humans and life threatening, systemic infections in immune compromised individuals. This proposal seeks to understand how C. albicans regulates its genes so it can survive and proliferate in many environments of its human host. An important component of our work is the identification of virulence genes which, in the long term, will provide molecular targets for new classes of antifungal drugs.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Project (R01)
Project #
4R01AI049187-15
Application #
8975112
Study Section
Pathogenic Eukaryotes Study Section (PTHE)
Program Officer
Duncan, Rory A
Project Start
2011-12-01
Project End
2017-11-30
Budget Start
2015-12-01
Budget End
2017-11-30
Support Year
15
Fiscal Year
2016
Total Cost
Indirect Cost

  Institution

Name
University of California San Francisco
Department
Microbiology/Immun/Virology
Type
Schools of Medicine
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94118

  Publications

Dalal, Chiraj K; Johnson, Alexander D (2017) How transcription circuits explore alternative architectures while maintaining overall circuit output. Genes Dev 31:1397-1405
Craik, Veronica B; Johnson, Alexander D; Lohse, Matthew B (2017) Sensitivity of White and Opaque Candida albicans Cells to Antifungal Drugs. Antimicrob Agents Chemother 61:
Lohse, Matthew B; Ene, Iuliana V; Craik, Veronica B et al. (2016) Systematic Genetic Screen for Transcriptional Regulators of the Candida albicans White-Opaque Switch. Genetics 203:1679-92
Lohse, Matthew B; Johnson, Alexander D (2016) Identification and Characterization of Wor4, a New Transcriptional Regulator of White-Opaque Switching. G3 (Bethesda) 6:721-9
Dalal, Chiraj K; Zuleta, Ignacio A; Mitchell, Kaitlin F et al. (2016) Transcriptional rewiring over evolutionary timescales changes quantitative and qualitative properties of gene expression. Elife 5:
Hernday, Aaron D; Lohse, Matthew B; Nobile, Clarissa J et al. (2016) Ssn6 Defines a New Level of Regulation of White-Opaque Switching in Candida albicans and Is Required For the Stochasticity of the Switch. MBio 7:e01565-15
Lohse, Matthew B; Kongsomboonvech, Pisiwat; Madrigal, Maria et al. (2016) Genome-Wide Chromatin Immunoprecipitation in Candida albicans and Other Yeasts. Methods Mol Biol 1361:161-84
Ene, Iuliana V; Lohse, Matthew B; Vladu, Adrian V et al. (2016) Phenotypic Profiling Reveals that Candida albicans Opaque Cells Represent a Metabolically Specialized Cell State Compared to Default White Cells. MBio 7:
Du, Han; Guan, Guobo; Li, Xiaoling et al. (2015) N-Acetylglucosamine-Induced Cell Death in Candida albicans and Its Implications for Adaptive Mechanisms of Nutrient Sensing in Yeasts. MBio 6:e01376-15
Mancera, Eugenio; Porman, Allison M; Cuomo, Christina A et al. (2015) Finding a Missing Gene: EFG1 Regulates Morphogenesis in Candida tropicalis. G3 (Bethesda) 5:849-56

Showing the most recent 10 out of 46 publications