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An Ex vivo Assay to Study Candida albicans Hyphal Morphogenesis in the Gastrointestinal Tract
07:42

An Ex vivo Assay to Study Candida albicans Hyphal Morphogenesis in the Gastrointestinal Tract

Published on: July 1, 2020

Inhibition of the pathogenically related morphologic transition in Candida albicans by disrupting Cdc42 binding to

Zhengding Su1, Hongjian Li, Yang Li

  • 1Biotechnology Research Institute, National Research Council of Canada, Montreal, Quebec H4P 2R2, Canada. z2su@uwaterloo.ca

Chemistry & Biology
|November 21, 2007
PubMed

Insights

Inhibiting Candida albicans Cdc42 (CaCdc42) with CRIB polypeptides reversed its pathogenic yeast-to-hyphal transition. This discovery offers a novel antifungal strategy by disrupting key protein interactions in disease pathways.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • The yeast-to-hyphal transition in *Candida albicans* is a critical factor in its pathogenicity as a human fungal pathogen.
  • This morphologic switch is controlled by complex cell signal transduction pathways, including those involving the small GTPase *Candida albicans* Cdc42 (CaCdc42).
  • CaCdcd42 interacts with downstream effectors possessing CRIB domains, such as CaCla4 and Cst20, to regulate this transition.

Purpose of the Study:

  • To investigate the potential of inhibiting CaCdcd42 activity in *Candida albicans*.
  • To explore the therapeutic implications of disrupting CaCdcd42-effector interactions for controlling fungal pathogenicity.
  • To advance the concept of signal transduction therapy for antifungal drug development.

Main Methods:

  • Utilizing peptide-mediated transduction to deliver CRIB polypeptides *in vivo* within *Candida albicans* cells.
  • Assessing the impact of CRIB polypeptide delivery on CaCdcd42 activity and downstream signaling.
  • Monitoring the morphologic state of *Candida albicans* (yeast vs. hyphal) following inhibition.

Main Results:

  • *In vivo* inhibition of CaCdcd42 was successfully achieved using peptide-mediated transduction of CRIB polypeptides.
  • The inhibition of CaCdcd42 effectively inactivated the pathogenic yeast-to-hyphal morphologic transition.
  • In some instances, the inhibition led to a reversal of the established pathogenic morphologic state.

Conclusions:

  • Disrupting protein-protein interactions within signal transduction pathways, specifically targeting CaCdcd42, presents a viable strategy for antifungal intervention.
  • Signal transduction therapy, by interfering with key molecular pathways, offers a promising new avenue for antifungal drug design and treatment.
  • This approach holds potential not only for *Candida albicans* infections but also for other diseases driven by aberrant signal transduction.

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