Hsp90-dependent regulatory circuitry controlling temperature-dependent fungal development and virulence.
The pathogenic fungi Candida albicans, Aspergillus fumigatus, and Cryptococcus neoformans are an increasing cause of human mortality, especially in immunocompromised populations. During colonization and adaptation to various host environments, these fungi undergo morphogenetic alterations that allow for survival within the host. One key environmental cue driving morphological changes is external temperature. The Hsp90 chaperone protein provides one mechanism to link temperature with the signalling cascades that regulate morphogenesis, fungal development and virulence. Candida albicans is a model system for understanding the connections between morphogenesis and Hsp90. Due to the high degree of conservation in Hsp90, many of the connections in C. albicans may be extrapolated to other fungal pathogens or parasites. Examining the role of Hsp90 during development and morphogenesis in these three major fungal pathogens may provide insight into key aspects of adaptation to the host, leading to additional avenues for therapy.
Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Teresa R
TR
O'Meara
Leah E
LE
Cowen
D001232:Aspergillus fumigatus / Q000166:cytology / Q000472:pathogenicity / Q000502:physiology / Q000528:radiation effects; D002176:Candida albicans / Q000166:cytology / Q000472:pathogenicity / Q000502:physiology* / Q000528:radiation effects*; D003455:Cryptococcus neoformans / Q000166:cytology / Q000472:pathogenicity / Q000502:physiology / Q000528:radiation effects; D015966:Gene Expression Regulation, Fungal; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism*; D013696:Temperature; D014774:Virulence
D018841:HSP90 Heat-Shock Proteins