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An Ex vivo Assay to Study Candida albicans Hyphal Morphogenesis in the Gastrointestinal Tract
Published on: July 1, 2020
Candida albicans transcription factor Rim101 mediates pathogenic interactions through cell wall functions.
Clarissa J Nobile1, Norma Solis, Carter L Myers
1Department of Microbiology, Columbia University, New York, NY, USA.
Cellular Microbiology
|July 17, 2008
Summary
Candida albicans Rim101 is essential for oral infection, independent of cell shape. Rim101 regulates cell wall genes, which restore virulence in a mutant lacking Rim101.
Area of Science:
- Mycology
- Pathogen Biology
- Molecular Genetics
Background:
- The Rim101/PacC family of pH-responsive transcription factors is crucial for fungal pathogen virulence.
- The precise mechanisms linking Rim101/PacC function to infection remain incompletely understood.
- Candida albicans Rim101 is a key regulator implicated in fungal pathogenesis.
Purpose of the Study:
- To investigate the role of Candida albicans Rim101 in oropharyngeal candidiasis.
- To identify Rim101 target genes and elucidate their contribution to virulence.
- To determine if Rim101's role in oral infection is linked to morphological changes.
Main Methods:
- Utilized an oropharyngeal candidiasis mouse model to assess Candida albicans virulence.
- Generated an nrg1 deletion mutant (nrg1Δ/Δ) to study Rim101 targets independently of the yeast-hypha transition.
- Employed an overexpression-rescue approach to analyze the function of identified Rim101 target genes.
Main Results:
- Rim101 is required for Candida albicans virulence in the oropharyngeal candidiasis model.
- Virulence in this model is independent of the yeast-hypha morphological transition.
- Increased expression of Rim101 target genes (ALS3, CHT2, PGA7/RBT6, SKN1, ZRT1) partially restored pathogenicity of a rim101Δ/Δ mutant.
- Four of the five identified genes are involved in cell wall structure.
Conclusions:
- Rim101-dependent alterations in cell wall composition contribute to Candida albicans pathogenesis in oral epithelial cells.
- This contribution is independent of fungal cell morphology.
- Rim101 regulates key virulence factors involved in host-pathogen interactions.
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