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MBC in Press, published online ahead of print August 15, 2007
Mol. Biol. Cell 10.1091/mbc.E07-05-0485

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Submitted on May 23, 2007
Revised on July 30, 2007
Accepted on August 6, 2007

Protein Kinase A and Sch9 Cooperatively Regulate Induction of Autophagy in Saccharomyces cerevisiae

Tomohiro Yorimitsu,* Shadia Zaman,{dagger} James R. Broach,{dagger} and Daniel J. Klionsky*

*Life Sciences Institute and Departments of Molecular, Cellular, and Developmental Biology and Biological Chemistry, University of Michigan, Ann Arbor, MI 48109; {dagger}Department of Molecular Biology, Princeton University, Princeton, NJ 08544

Monitoring Editor: Janet Shaw

Autophagy is a highly conserved, degradative process in eukaryotic cells. The rapamycin-sensitive Tor kinase complex 1 (TORC1) has a major role in regulating induction of autophagy; however, the regulatory mechanisms are not fully understood. Here, we find that the protein kinase A (PKA) and Sch9 signaling pathways regulate autophagy cooperatively in yeast. Autophagy is induced in cells when PKA and Sch9 are simultaneously inactivated. Mutant alleles of these kinases bearing a mutation that confers sensitivity to the ATP-analog inhibitor, 1NM-PP1, revealed that autophagy was induced independent of effects on Tor kinase. The PKA-Sch9-mediated autophagy depends on the Atg1 kinase complex, which is also essential for TORC1-regulated autophagy, the transcription factors Msn2/4 and the Rim15 kinase. The present results suggest that autophagy is controlled by the signals from at least three partly separate nutrient-sensing pathways that include PKA, Sch9 and TORC1.

Address correspondence to: Daniel J. Klionsky (klionsky{at}umich.edu)






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