Deletions of the endocytic components VPS28 and VPS32 in Candida albicans lead to echinocandin and azole hypersensitivity

Antimicrob Agents Chemother. 2006 Oct;50(10):3492-5. doi: 10.1128/AAC.00391-06.

Abstract

Vps28p and Vps32p act in both the endocytic and the pH signaling pathways in yeasts and are required for Candida albicans virulence. Here, we show that deletions of VPS28 and VPS32 increase the susceptibility of C. albicans to cell wall disruption agents, echinocandin and azole antifungal agents.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antifungal Agents / pharmacology*
  • Azoles / pharmacology
  • Candida albicans / drug effects*
  • Candida albicans / genetics
  • Caspofungin
  • Echinocandins
  • Endocytosis
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism
  • Gene Deletion*
  • Gene Expression Regulation, Fungal
  • Lipopeptides
  • Lipoproteins / pharmacology
  • Micafungin
  • Microbial Sensitivity Tests
  • Nuclear Proteins / genetics*
  • Nuclear Proteins / metabolism
  • Peptides, Cyclic / pharmacology
  • Vesicular Transport Proteins / genetics*
  • Vesicular Transport Proteins / metabolism

Substances

  • Antifungal Agents
  • Azoles
  • Echinocandins
  • Fungal Proteins
  • Lipopeptides
  • Lipoproteins
  • Nuclear Proteins
  • Peptides, Cyclic
  • Vesicular Transport Proteins
  • Caspofungin
  • Micafungin