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Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
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Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis

Published on: March 19, 2019

Candida albicans Ecm33p is important for normal cell wall architecture and interactions with host cells

Raquel Martinez-Lopez1, Hyunsook Park, Carter L Myers

  • 1Departamento de Microbiología II, Facultad de Farmacia, Universidad Complutense de Madrid, Spain.

Eukaryotic Cell
|January 10, 2006
PubMed

Insights

Candida albicans ECM33 protein is crucial for cell wall integrity and virulence. Deleting ECM33 impairs fungal growth, adherence, invasion, and damages host cells, affecting cell wall structure and surface protein localization.

Area of Science:

  • Mycology
  • Cell Biology
  • Infectious Diseases

Background:

  • Candida albicans is an opportunistic fungal pathogen.
  • The cell wall is essential for fungal survival and virulence.
  • ECM33 is a glycosylphosphatidylinositol-anchored mannoprotein in the C. albicans cell wall.

Purpose of the Study:

  • Investigate the role of ECM33 in C. albicans virulence.
  • Elucidate the mechanisms by which Ecm33p contributes to fungal-host interactions.
  • Analyze the impact of ECM33 deletion on cell wall integrity and host cell invasion.

Main Methods:

  • Generating C. albicans ecm33 deletion mutants (ecm33Delta).
  • Assessing fungal growth rates and hyphal formation in vitro.
  • Evaluating fungal adherence, invasion, and damage to endothelial and oral epithelial cells.
  • Utilizing transmission electron microscopy to examine cell wall ultrastructure.
  • Expressing C. albicans ECM33 in Saccharomyces cerevisiae to test Ecm33p function.

Main Results:

  • ECM33 deletion mutants exhibited a 50% slower blastospore growth rate.
  • Mutants showed reduced adherence to, invasion of, and damage to host cells.
  • Hyphal formation and length were unaffected by ECM33 deletion.
  • Transmission electron microscopy revealed an electron-dense outer mannoprotein layer in mutant cell walls.
  • Aberrant surface localization of the adhesin Als1p was observed in mutant hyphae.
  • Saccharomyces cerevisiae expressing ECM33 did not exhibit adherence or invasion.

Conclusions:

  • Ecm33p is essential for maintaining normal cell wall architecture in C. albicans.
  • ECM33 plays a critical role in fungal virulence by influencing cell wall integrity and host cell interactions.
  • Ecm33p is required for proper function and localization of cell surface proteins, such as Als1p.
  • ECM33 is a potential target for antifungal therapies aimed at disrupting C. albicans virulence.

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