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Modulation of histone H3 lysine 56 acetylation as an antifungal therapeutic strategy

Hugo Wurtele1, Sarah Tsao, Guylaine Lépine

  • 1Institute for Research in Immunology and Cancer, Université de Montréal, Montreal, Canada.

Nature Medicine
|July 6, 2010
PubMed

Insights

Modulating histone H3 Lys56 acetylation (H3K56ac) in Candida albicans, a key fungal pathogen, offers a novel antifungal strategy. Targeting H3K56ac levels can reduce infection virulence and sensitize yeast to treatments.

Area of Science:

  • Mycology
  • Molecular Biology
  • Epigenetics

Background:

  • Candida albicans is a significant opportunistic fungal pathogen.
  • Histone modifications, like H3K56ac, are crucial for yeast cellular processes.
  • Fungal-specific enzymes regulating H3K56ac present potential antifungal drug targets.

Purpose of the Study:

  • To investigate the role of H3K56ac in Candida albicans.
  • To identify the genes regulating H3K56ac in C. albicans.
  • To evaluate the therapeutic potential of modulating H3K56ac levels.

Main Methods:

  • Gene expression analysis of RTT109 and HST3.
  • Assessment of H3K56ac levels.
  • Sensitivity assays with genotoxic and antifungal agents.
  • Phenotypic analysis including cell viability and DNA staining.
  • Virulence testing in a mouse infection model.

Main Results:

  • H3K56ac in C. albicans is regulated by Rtt109p (acetyltransferase) and Hst3p (deacetylase).
  • Reduced H3K56ac sensitizes C. albicans to antifungal and genotoxic agents.
  • Inhibition of Hst3p leads to cell death, abnormal growth, and DNA aberrations.
  • Altering H3K56ac levels reduces C. albicans virulence in vivo.

Conclusions:

  • H3K56ac is a critical epigenetic mark in C. albicans.
  • Modulation of H3K56ac represents a promising therapeutic strategy against C. albicans infections.
  • This approach may also be applicable to other fungal pathogens.

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