Figure 5.

IMS redox pathways exert only a limited influence on E_GSH[IMS]. (A) Steady states of the cytosolic and mitochondrial sensors (Grx1-roGFP2, Su9-Grx1-roGFP2, b₂-Grx1-roGFP2) in wt cells grown on galactose (Gal) or glycerol (Glyc). Experiment was performed as described in Figure 1C. Reported values are the mean of three independent experiments. Error bars are the means±s.d. (B) Recovery kinetics after diamide shock in wt cells grown on galactose or glycerol. Cells expressing Grx1-roGFP2, Su9-Grx1-roGFP2 and b₂-Grx1-roGFP2 were analysed as described in Figure 1F. Reported values are the mean of three independent experiments. Error bars are the means±s.d. (C) Scheme of the investigated IMS redox pathways. (D) Scheme depicting the three parameters to evaluate the recovery kinetics after oxidative shock: (i) apparent lag phase, (ii) recovery rate and (iii) steady-state OxD. For full description, see Supplementary Figure S2. (E) Qualitative representation of the results obtained from the analysis of (i) chemical treatments to inhibit complexes of the respiratory chain (antimycin A (AntA), potassium cyanide (KCN) to inhibit complexes III and IV, respectively, and paraquat to induce mitochondrial oxidative stress), (ii) mutants that result in defective respiratory chain complexes (Δrip1, Δcox17, Δnde1 and Δnde2), (iii) deletions of enzymes counteracting ROS (Δsod1, Δsod2, Δccp1) and (iv) strains that express Erv1 and Mia40 under the control of regulatable promoters. The full set of data is presented in Supplementary Figures S4–S8, respectively.