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. 2018 May 23;26(3):487–501. doi: 10.1038/s41418-018-0133-4

Fig. 5.

Fig. 5

O2 consumption and COX activity are impaired in cnb1∆ and ire1∆ cells. a Left panel, O2 consumption by cells grown overnight to mid-log phase in FK506 (2 µg/mL) were compared with that of wild-type and cnb1∆ cells. Right panel, COX activity measured in isolated mitochondria as oxidation of cytochrome c. b O2 consumption in ire1∆ cells is not entirely attributable to oxidative phosphorylation. O2 consumption was measured in wild-type, cnb1∆, and ire1∆ cells. Cells were treated with TET (10 mM) to inhibit ATP synthase; O2 consumption in wild-type and cnb1∆, but not ire1∆ cells falls to 0. Addition of CCCP (10 µM) induces O2 consumption to return to maximal. c Reduced ETC activity in ire1∆ cells. Left panel, O2 consumption by oxidative phosphorylation (TET-inhibitable) in wild-type, cnb1∆ and ire1∆ cells. Right panel, COX activity was measured in isolated mitochondria. Wild-type cells were grown to mid-log phase overnight in SC with 3% glycerol for comparison with strains grown in SC with 2% glucose.