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. 2007 Oct;18(10):4180–4189. doi: 10.1091/mbc.E07-05-0485

Figure 3.

Figure 3.

Atg1 kinase activity is required for PKA-Sch9 regulation of autophagy. (A) Inactivation of PKA and Sch9 does not induce autophagy without the Atg1–Atg13–Atg17 kinase complex. Protein extracts from wild-type and pka pkb strains, and these strains harboring deletions in ATG1, ATG13, or ATG17 and expressing GFP-Atg8 were subjected to immunoblotting, as described in Figure 1. An Atg17 mutant defective in association with Atg13 (B) and a kinase-defective Atg1 mutant (C) block autophagy when PKA and Sch9 are inactivated. Protein extracts from the atg17Δ pka sch9 (TYY191) (B) or atg1Δ pka sch9 (TYY167) (C) cells harboring the empty vector, and a plasmid expressing wild-type Atg17 or the Atg17C24R mutant (B) or wild-type Atg1 or the Atg1K54A mutant (C) were subjected to immunoblotting, as described in A. (D) atg1Δ sch9 (TYY166) and atg1Δ pka sch9 cells harboring the empty vector, or a plasmid expressing wild-type Atg1 or the Atg1S508,515A mutant (AA) were grown and TCA-precipitated proteins were subjected to immunoblotting, as described in A.