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Published on: October 18, 2017
Wild-type Drosophila melanogaster as a model host to analyze nitrogen source dependent virulence of Candida albicans
Monica M Davis1, Francisco J Alvarez, Kicki Ryman
1Department of Molecular Biology and Functional Genomics, Stockholm University, Stockholm, Sweden.
Abstract:
The fungal pathogen Candida albicans is a common cause of opportunistic infections in humans. We report that wild-type Drosophila melanogaster (OrR) flies are susceptible to virulent C. albicans infections and have established experimental conditions that enable OrR flies to serve as model hosts for studying C. albicans virulence. After injection into the thorax, wild-type C. albicans cells disseminate and invade tissues throughout the fly, leading to lethality. Similar to results obtained monitoring systemic infections in mice, well-characterized cph1Δ efg1Δ and csh3Δ fungal mutants exhibit attenuated virulence in flies. Using the OrR fly host model, we assessed the virulence of C. albicans strains individually lacking functional components of the SPS sensing pathway. In response to extracellular amino acids, the plasma membrane localized SPS-sensor (Ssy1, Ptr3, and Ssy5) activates two transcription factors (Stp1 and Stp2) to differentially control two distinct modes of nitrogen acquisition (host protein catabolism and amino acid uptake, respectively). Our results indicate that a functional SPS-sensor and Stp1 controlled genes required for host protein catabolism and utilization, including the major secreted aspartyl protease SAP2, are required to establish virulent infections. By contrast, Stp2, which activates genes required for amino acid uptake, is dispensable for virulence. These results indicate that nutrient availability within infected hosts directly influences C. albicans virulence.
Insights
Candida albicans virulence relies on its ability to sense and utilize host nutrients. The SPS sensing pathway, particularly Stp1, is crucial for C. albicans to break down host proteins for virulent infections.
Area of Science:
- Microbiology
- Mycology
- Infectious Diseases
Background:
- Candida albicans is a significant opportunistic fungal pathogen causing human infections.
- Understanding the molecular mechanisms of C. albicans virulence is critical for developing effective treatments.
Purpose of the Study:
- To establish a Drosophila melanogaster (fruit fly) model for studying C. albicans virulence.
- To investigate the role of the SPS sensing pathway in C. albicans pathogenesis.
Main Methods:
- Utilized wild-type and mutant strains of C. albicans.
- Infected Drosophila melanogaster (OrR strain) with C. albicans.
- Assessed fungal mutant virulence and gene expression related to nutrient acquisition.
Main Results:
- Drosophila melanogaster serves as a viable model host for C. albicans infection studies.
- The SPS sensing pathway, specifically the Stp1 transcription factor, is essential for C. albicans virulence.
- Stp1 controls genes for host protein catabolism (e.g., SAP2), which are required for virulence.
- Stp2, involved in amino acid uptake, is not essential for virulence in this model.
Conclusions:
- Nutrient availability and utilization pathways significantly impact C. albicans virulence.
- The fruit fly model effectively recapitulates key aspects of C. albicans pathogenesis.
- Targeting host protein catabolism pathways could be a strategy to combat C. albicans infections.
