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. 2015 Jun 9;5:290–300. doi: 10.1016/j.redox.2015.06.002

Fig. 7.

Fig. 7

The Regulation of Protein ubiquitination through Sch9 signaling during growth. A speculative model of how reduced Sch9 signaling down-regulated ubiquitinated proteins by Rim15-dependent stress-resistance pathways (left arm) and adaptive mitochondrial ROS signaling (right arm). Elevated respiration in sch9∆ cells is mediated by upregulation of the transcription factors Hap4 or Hcm1 which gives rise to increased respiration and intracellular superoxide during growth [32,33]. Superoxide may serve as an adaptive signal to activate stress response genes (horizontal arrow). Therefore, although elevated cellular superoxide leads to accumulated H2O2, enhanced stress Resistance via Rim15 pathway and adaptive superoxide signal [30], on the other hand, diminishes H2O2 more effectively (bold arrow). Elimination of H2O2 in sch9∆ cells in turn reduces the oxidation of intracellular proteins including those of newly synthesized and their subsequent ubiquitination.