Fig. 6: Ate1-induced cell death involves mitochondrial permeabilization transition pore.
From: Arginyltransferase1 drives a mitochondria-dependent program to induce cell death
A A diagram showing some of the key components in yeasts that affect mitochondrial permeabilization transition pore (mPTP) and apoptosis. Note that the Bcl-XL is not an endogenous protein of yeast, but it can interact with the mitochondrial outer membrane permeabilization (MOMP) event [56]. B Growth of yeast cells (WT, aac1Δ, aac2Δ¸ aac3Δ, all on W303 strains) carrying either the empty expression vector (vector) or pGAL1:ATE1-GFP (+Ate1-GFP) was measured by a serial dilution growth assay on either plate containing 2% glucose or 2% galactose, where the expression of Ate1 is not induced or induced, respectively. Plates were incubated at 30 °C and images were taken after 2–3 days. C Similar to (B), except that WT and mir1Δ yeasts were used. D Serial dilution growth assay to assess changes in growth of WT yeast induced with pGAL: Ate1-GFP in the context of various ATP synthase inhibitors. Yeasts were grown in raffinose-containing liquid media before being washed, serially diluted in H20, and plated to either glucose or galactose-containing plates with the designated concentrations of inhibitors, including Oligomycin A, Quercetin, and α-ketoglutarate (α-KG). Plates were allowed to grow three days before images were taken. DMSO (at a final concentration of 0.004% in the plate) was used as vehicle control. See also Suppl Fig. S1B to see the equal growth rate of the involved mutant yeast strains carrying the empty vector on galactose-containing media, compared to the WT strain.
