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Updated: May 13, 2026
Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
Published on: March 19, 2019
Cell surface changes in the Candida albicans mitochondrial mutant goa1Δ are associated with reduced recognition by
Xiaodong She1, Lulu Zhang, Hui Chen
1Department of Microbiology & Immunology, Georgetown University Medical Center, Washington DC 20057, USA.
Abstract:
We have previously characterized several fungal-specific proteins from the human pathogen Candida albicans that either encode subunits of mitochondria Complex I (CI) of the electron transport chain (ETC) or regulate CI activity (Goa1p). Herein, the role of energy production and cell wall gene expression is investigated in the mitochondria mutant goa1Δ. We show that downregulation of cell wall-encoding genes in the goa1Δ results in sensitivity to cell wall inhibitors such as Congo red and Calcofluor white, reduced phagocytosis by a macrophage cell line, reduced recognition by macrophage receptors, and decreased expression of cytokines such as IL-6, IL-10 and IFN-γ. In spite of the reduced recognition by macrophages, the goa1Δ is still killed to the same extent as control strains. We also demonstrate that expression of the epithelial cell receptors E-cadherin and EGFR is also reduced in the presence of goa1Δ. Together, our data demonstrate the importance of mitochondria in the expression of cell wall biomolecules and the interaction of C. albicans with innate immune and epithelial cells. Our underlying premise is thatmitochondrial proteins such as Goa1p and other fungal-specific mitochondrial proteins regulate critical functions in cell growth and in virulence. As such, they remain as valid drug targets for antifungal drug discovery.
Insights
Mitochondria protein Goa1p impacts Candida albicans virulence. Its absence disrupts cell wall integrity, affecting interactions with immune and epithelial cells, highlighting potential antifungal drug targets.
Area of Science:
- Mycology
- Cell Biology
- Immunology
Background:
- Candida albicans is a human pathogen.
- Mitochondrial proteins, including Goa1p, are crucial for fungal survival and virulence.
- Mitochondria Complex I (CI) and its regulation are key to energy production.
Purpose of the Study:
- To investigate the role of mitochondria and Goa1p in Candida albicans cell wall gene expression and virulence.
- To understand how mitochondrial dysfunction affects the interaction of C. albicans with host cells.
Main Methods:
- Created a goa1Δ mutant of Candida albicans.
- Analyzed cell wall gene expression.
- Assessed sensitivity to cell wall inhibitors (Congo red, Calcofluor white).
- Evaluated phagocytosis by macrophages and cytokine expression (IL-6, IL-10, IFN-γ).
- Measured expression of epithelial cell receptors (E-cadherin, EGFR).
Main Results:
- The goa1Δ mutant showed downregulated cell wall genes, leading to sensitivity to cell wall inhibitors.
- Phagocytosis by macrophages and recognition by macrophage receptors were reduced.
- Expression of cytokines IL-6, IL-10, and IFN-γ decreased.
- Epithelial cell receptor expression (E-cadherin, EGFR) was also reduced.
- Despite reduced recognition, the goa1Δ mutant was killed by macrophages similarly to controls.
Conclusions:
- Mitochondria play a critical role in regulating cell wall biomolecule expression in Candida albicans.
- Mitochondrial function, specifically involving Goa1p, is essential for C. albicans interactions with innate immune and epithelial cells.
- Fungal-specific mitochondrial proteins like Goa1p are potential drug targets for antifungal therapies.
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