Mitochondrial fusion and fission are involved in stress tolerance of Candida glabrata

Abstract

Background: Recently, cell tolerance toward environmental stresses has become the major problem in the development of industrial microbial fermentation. Acetoin is an important chemical that can be synthesized by microbes. Its toxicity was investigated using Candida glabrata as the model in this study. Results: A series of physiological and biochemical experiments demonstrated that the organic solvent acetoin can inhibit cell growth by increasing intracellular reactive oxygen species (ROS) production and inducing damage to mitochondria and cell apoptosis. Integrating RT-PCR experiments, the genes fzo1 and dnm1 were overexpressed to regulate the balance between mitochondrial fusion and fission. Enhancement of mitochondrial fusion was shown to significantly increase cell tolerance toward acetoin stress by inhibiting ROS production and increasing the intracellular adenosine triphosphate (ATP) supply, which was also demonstrated by the addition of citrate. Conclusions: Regulating mitochondrial fusion-fission may be an alternative strategy for rationally improving the growth performance of eukaryotes under high environmental stress conditions, and also expands our knowledge of the mechanisms of cell tolerance through the processes of energy-related metabolic pathways.