ИСТИНА

Xenobiotics or environmental stresses can induce secondary oxidative stress in yeast cells [1]. In this case, cell survival depends on the activation of antioxidant systems. Importantly, cytoplasm and mitochondrial matrix harbor different ROS-scavenging enzymes. We studied the contribution of cytoplasmic (SOD1) and mitochondrial (SOD2) superoxide dismutases to yeast stress resistance. The repression of SOD1 but not SOD2 had a significant effect on yeast survival in the presence of prooxidants menadione and paraquat. At the same time, the contribution of SOD2 was much more pronounced in cells treated with low-molecular weight alcohols. The deletion of SOD2 but not SOD1 prevented activation of Yap1p, a hydrogen peroxide-sensing transcription factor. Sod2p contributes to generation of hydrogen peroxide in mitochondrial matrix. Hydrogen peroxide, unlike superoxide anion, can penetrate mitochondrial inner membrane and activate cytosolic ROS sensors. We showed a positive epistatic interaction between yap1 and sod2 deletions under acute ethanol stress [2]. This suggests that Sod2p and Yap1p act as a module of a mitochondria-to-nucleus signaling pathway. Moreover, this pathway was negatively regulated by another retrograde signaling route comprising Rtg proteins. Together our data suggest a signaling role of mitochondrial superoxide dismutase in yeast. We speculate that mitochondria-to-nucleus pathways interfere with each other to ensure specificity of compensatory transcriptional response (see for discussion [3]). This work was supported by the Russian Science Foundation (project No. 14-24-00107)