Fig 8. Overexpression of Pde2p can rescue the petite-negative phenotype of several mutants defective for mitochondrial function.

(A) High-copy Pde2p can allow mutants deficient in activity of the i-AAA protease to remain viable following mtDNA loss. Strains BY4741 (WT), CDD13 (mgr1Δ), and CDD15 (mgr3Δ) were treated as in Fig 1A, with additional incubation of ρ⁰ cells to 4 d in order to demonstrate suppression of the petite-negative phenotype. (B) PKA inhibition by Pde2p overexpression can rescue the petite-negative phenotype of mutants deficient in mitochondrial protein import and assembly. Strains BY4741 (WT), CDD11 (mgr2Δ), and CDD17 (phb1Δ) were treated as in (A). (C) Overexpression of Pde2p allows cells lacking mtDNA to proliferate in the absence of F₁-ATPase activity. Strains CDD463 (WT) and CDD215 (atp2Δ) were treated as in Fig 1A, with further incubation of ρ⁰ cells to 6 d.