Mechanisms of White-Opaque Switching in Candida albicans

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Principal Investigator: ALEXANDER D JOHNSON
Organization: UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
Fiscal Year: 2024
Award: $727,285
Funding agency: National Institute of Allergy and Infectious Diseases

Project Summary/Abstract
Candida albicans is one of the most prevalent fungal pathogen of humans and also a component of
the human microbiome; it can cause superficial infections in normal humans and life-threatening
systemic infections in immune compromised individuals. Our work seeks to understand how C.
albicans regulates its genes so it can survive and proliferate in the many different environments of its
human host. This proposal focuses on a single, large transcription circuit—the white-opaque switching
circuit—which allows two different cell-types to be produced epigenetically from the same genome.
White-opaque switching is deeply conserved across clinical isolates of C. albicans and is also
observed in closely related Candida species. This proposal seeks to understand the mechanism
behind white-opaque switching, the mechanisms underlying the stability of the two distinct, epigenetic
cell-types and the effects of white-opaque switching on Candida’s ability to thrive in its mammalian
hosts.

Terms: <Accounting><Affect><Alimentary Canal><Assay><Auxins><Behavior><Bioassay><Biological Assay><Biological Function><Biological Process><C albicans><C. albicans><C.albicans><Candida><Candida albicans><Cell Body><Cell division><Cells><Clinical><DNA Modification><DNA Modification Process><Data><Devices><Digestive Tract><Disease><Disorder><Environment><Epigenetic><Epigenetic Change><Epigenetic Mechanism><Epigenetic Process><Event><Feedback><Fluorescence><Fluorescence Light Microscopy><Fluorescence Microscopy><GI Tract><GI colonization><Gastrointestinal Tract><Gastrointestinal tract structure><Gene Transcription><Generalized Growth><Generations><Genes><Genetic Transcription><Genome><Goals><Growth><Human><Human Microbiome><Immune><Immunes><In Vitro><Individual><Infection><Injections><Laboratories><Life><Maintenance><Mammalia><Mammals><Memory><Mice><Mice Mammals><Microfluidics><Modeling><Modern Man><Molecular><Monilia><Morphology><Mucosa><Mucosal Tissue><Mucous Membrane><Murine><Mus><Organism><Oropharyngeal Candidiasis><Patients><Play><Proliferating><RNA Expression><Regulation><Reporter><Role><Series><Sterility><Symbiosis><System><Systemic infection><Tail><Technology><Testing><Time><Tissue Growth><Transcription><Veins><Virulence><Work><Yeasts><alimentary tract><burden of disease><burden of illness><cell type><clinical relevance><clinically relevant><commensalism><digestive canal><disease burden><epigenetically><fungal pathogen><fungi pathogen><gastrointestinal tract colonization><gut colonization><histone modification><human pathogen><human-associated microbiome><intestinal colonization><living system><mouse model><murine model><mutant><ontogeny><oropharyngeal thrush><pathogenic fungus><response><social role><sterile><µfluidic>