Involvement of HOG1 MAPK in the regulation of sodium arsenite-induced apoptosis in yeast cells

Abstract:

[Objective] In this study, we studied the role of HOG1 MAPK in sodium arsenite-induced apoptosis in yeast cells. [Methods] Yeast wild-type (BY4741) and HOG1 mutant (ΔHOG1) strains were used to study the effects of sodium arsenite on the growth and relative survival rate and oxidative damages of yeast cells. Further, the apoptotic rate, intracellular reactive oxygen species (ROS) level, and mitochondrial membrane potential of the yeast cells under sodium arsenite-induced stress were determined by flow cytometry. [Results] Sodium arsenite inhibited the growth of yeast cells and induced their apoptosis. Compared to the wild-type strain in the same treatment group, ΔHOG1 strain showed higher sensitivity to sodium arsenite with a lower cell survival rate and higher apoptotic rate. Under sodium arsenite-induced stress, ΔHOG1 strain showed significantly higher intracellular ROS and malondialdehyde (MDA) levels than the wild-type BY4741 strain. On the contrary, the mitochondrial membrane potential of ΔHOG1 strain was significantly lower than that of the wild-type BY4741 strain. [Conclusion] These results indicated that HOG1 MAPK gene was involved in the regulation of sodium arsenite-induced apoptosis by affecting intracellular ROS level and changing △ψ_M in yeast cells.