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Int J Med Microbiol. 2002 Oct;292(5-6):299-311.

Co-regulation of pathogenesis with dimorphism and phenotypic switching in Candida albicans, a commensal and a pathogen.

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Department of Biological Chemistry, University of California, Irvine, Irvine, CA 92697-1700, USA. H4LIU@UCI.EDU


Candida albicans, a common fungal pathogen of humans, can colonize in many diverse environments of the host and convert between a harmless commensal and a pathogen. Recent advances indicate that C. albicans uses a common set of conserved pathways to regulate dimorphism, mating and phenotypic switching. Major pathways known to regulate dimorphism include a mitogen-activated protein (MAP) kinase pathway through Cph1, the cAMP-dependent protein kinase pathway via Efg1, and Tup1-mediated repression through Rfg1 and Nrg1. The Cph1-mediated MAP kinase pathway is critical for the mating process, while all three pathways are implicated in the regulation of white-opaque switching. All these developmental pathways regulate the expression of hypha-specific and/or phase-specific genes. A high proportion of hypha-specific genes and phase-specific genes encode proteins that contribute directly or indirectly to pathogenesis and virulence of C. albicans. Therefore, virulence genes are co-regulated with cell morphogenesis. This supports a previous notion that the unique aspects of C. albicans commensalism and pathogenesis may lie in the developmental programs of dimorphism and phenotypic switching.

[Indexed for MEDLINE]

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