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Published on: June 19, 2013
Detection and measurement of two-component systems that control dimorphism and virulence in fungi
Julie C Nemecek1, Marcel Wüthrich, Bruce S Klein
1Department of Pediatrics, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
Abstract:
Systemic dimorphic fungi include six phylogenetically related ascomycetes. These organisms grow in a mold form in the soil on most continents around the world. After the mold spores, which are the infectious particles, are inhaled into the lung of a susceptible mammalian host, they undergo a morphological change into a pathogenic yeast form. The ability to convert to the yeast form is essential for this class of fungal agents to be pathogenic and produce disease. Temperature change is one key stimulus that triggers the phase transition from mold (25 degrees ) to yeast (37 degrees ). Genes that are expressed only in the pathogenic yeast form of these fungi have been identified to help explain how and why this phase transition is required for virulence. However, the regulators of yeast-phase specific genes, especially of phase transition from mold to yeast, have remained poorly understood. We used Agrobacterium-mediated gene transfer for insertional mutagenesis to create mutants that are defective in the phase transition and to identify genes that regulate this critical event. We discovered that a hybrid histidine kinase senses environmental signals such as temperature and regulates phase transition, dimorphism, and virulence in members of this fungal family. This chapter describes our approach to the identification and analysis of this global regulator.
Insights
Researchers identified a hybrid histidine kinase that regulates the critical temperature-triggered transition from mold to pathogenic yeast form in systemic dimorphic fungi, impacting virulence. This discovery sheds light on fungal pathogenesis.
Area of Science:
- Mycology
- Medical Mycology
- Fungal Pathogenesis
Background:
- Systemic dimorphic fungi are ascomycetes that exist as molds in the environment and pathogenic yeasts in hosts.
- These fungi cause disease upon inhalation of mold spores, which convert to yeast form within the mammalian host.
- The morphological transition to the yeast form is crucial for fungal pathogenicity, with temperature being a key trigger.
Purpose of the Study:
- To identify and characterize the regulators of the mold-to-yeast phase transition in systemic dimorphic fungi.
- To understand the molecular mechanisms underlying fungal dimorphism and virulence.
- To investigate genes specifically expressed in the pathogenic yeast form.
Main Methods:
- Agrobacterium-mediated gene transfer was employed for insertional mutagenesis.
- Mutants defective in the mold-to-yeast phase transition were generated and analyzed.
- Identification of genes regulating the critical dimorphic transition event.
Main Results:
- A hybrid histidine kinase was discovered as a key regulator of fungal phase transition.
- This kinase senses environmental signals, including temperature, to control dimorphism.
- The identified kinase plays a role in regulating virulence in systemic dimorphic fungi.
Conclusions:
- Hybrid histidine kinases are global regulators of temperature-dependent dimorphism in systemic dimorphic fungi.
- Understanding these regulators is essential for developing strategies against fungal infections.
- This research provides insights into the molecular basis of fungal virulence and host-pathogen interactions.
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