Candida albicans cells lacking CaMCA1-encoded metacaspase show resistance to oxidative stress-induced death and change in energy metabolism

Fungal Genet Biol. 2009 Feb;46(2):183-9. doi: 10.1016/j.fgb.2008.11.001. Epub 2008 Nov 14.


Candida albicans, an opportunistic pathogen, can undergo programmed cell death upon various stimuli, including oxidative stress. In this study, we showed that deletion of CaMCA1, a homologue of Saccharomyces cerevisiae metacaspase YCA1, could both attenuated oxidative stress-induced cell death and caspase activation. Compared to wild-type strain, Camca1Delta mutant showed higher accumulation of trehalose and transcription of the genes related to trehalose biosynthesis (TPS2 and TPS3) under the condition of oxidative stress. Furthermore, lower intracellular ATP concentration and mitochondrial membrane potential, less endogenous reactive oxygen species (ROS) generation were observed in Camca1Delta mutant. Our results suggest that CaMCA1 might mediate the sensitiveness to oxidative stress by affecting energy metabolism in C. albicans.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Triphosphate / metabolism
  • Candida albicans / enzymology*
  • Candida albicans / genetics
  • Candida albicans / physiology
  • Caspases / genetics
  • Caspases / metabolism*
  • Energy Metabolism*
  • Enzyme Activation
  • Fungal Proteins / genetics
  • Fungal Proteins / metabolism*
  • Membrane Potential, Mitochondrial
  • Microbial Viability
  • Oxidative Stress*
  • Reactive Oxygen Species / metabolism
  • Sequence Deletion
  • Trehalose / metabolism


  • Fungal Proteins
  • Reactive Oxygen Species
  • Adenosine Triphosphate
  • Trehalose
  • Caspases