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Two negative regulators of biofilm development exhibit functional divergence in conferring virulence potential to

Pallavi Kakade1, Kasturi Mahadik1, Kithiganahalli Narayanaswamy Balaji1

  • 1Department of Microbiology and Cell Biology, Indian Institute of Science, C V Raman Avenue, New Biological Sciences Building, Bangalore 560012, India.

FEMS Yeast Research
|July 28, 2018
PubMed

Insights

Two transcription factors, Zcf32 and Upc2, negatively regulate Candida albicans biofilm formation. Zcf32 enhances virulence and inflammation, while Upc2 compromises virulence and promotes anti-inflammatory responses.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Mycology

Background:

  • Candida albicans possesses an expanded family of Zn(II)2Cys6 transcription factors, including Zcf32 and the conserved Upc2.
  • Zcf32 is a CTG clade-specific protein that is less understood compared to Upc2 in C. albicans.

Purpose of the Study:

  • To investigate the roles of Zcf32 and Upc2 in Candida albicans biofilm development and virulence.
  • To compare the functional divergence and resemblance between Zcf32 and Upc2.

Main Methods:

  • Construction and analysis of null mutants for Zcf32 and Upc2.
  • Biofilm formation assays.
  • Virulence assessment using a mouse model of candidiasis.
  • Analysis of host inflammatory responses (cytokine profiling).

Main Results:

  • Both zcf32 and upc2 null mutants exhibited enhanced biofilm formation compared to wild-type, indicating negative regulation.
  • Zcf32 and Upc2 target distinct sets of biofilm-related genes.
  • The zcf32/zcf32 mutant was hypervirulent, whereas the upc2/upc2 mutant showed reduced virulence in a mouse model.
  • Absence of Zcf32 exacerbated inflammation (TNFα, IFNβ, IFNγ), while absence of Upc2 led to elevated anti-inflammatory responses (IL4, IL10).

Conclusions:

  • Zcf32 and Upc2, despite functional similarities in biofilm regulation, exhibit distinct roles in C. albicans virulence and host immune interaction.
  • Zcf32, a recently evolved factor, shows functional divergence from the ubiquitous Upc2 in pathogen virulence mechanisms.

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