Tor Directly Controls the Atg1 Kinase Complex To Regulate Autophagy

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Veröffentlicht in:Molecular and Cellular Biology Jg. 30; H. 4; S. 1049 - 1058
Hauptverfasser: Kamada, Yoshiaki, Yoshino, Ken-ichi, Kondo, Chika, Kawamata, Tomoko, Oshiro, Noriko, Yonezawa, Kazuyoshi, Ohsumi, Yoshinori
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States American Society for Microbiology 01.02.2010
Taylor & Francis
American Society for Microbiology (ASM)
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ISSN:0270-7306, 1098-5549, 1098-5549
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Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.
Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via inactivation of the rapamycin-sensitive Tor complex1 (TORC1), a protein kinase complex regulating cell growth in response to nutrient conditions. However, the mechanism by which TORC1 controls autophagy and the direct target of TORC1 activity remain unclear. Atg13 is an essential regulatory component of autophagy upstream of the Atg1 kinase complex, and here we show that yeast TORC1 directly phosphorylates Atg13 at multiple Ser residues. Additionally, expression of an unphosphorylatable Atg13 mutant bypasses the TORC1 pathway to induce autophagy through activation of Atg1 in cells growing under nutrient-rich conditions. Our findings suggest that the direct control of the Atg1 complex by TORC1 induces autophagy.
Author Chika Kondo
Noriko Oshiro
Tomoko Kawamata
Ken-ichi Yoshino
Kazuyoshi Yonezawa
Yoshinori Ohsumi
Yoshiaki Kamada
AuthorAffiliation Division of Molecular Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan, 1 Biosignal Research Center, Kobe University, Kobe 657-8501, Japan 2
AuthorAffiliation_xml – name: Division of Molecular Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan, 1 Biosignal Research Center, Kobe University, Kobe 657-8501, Japan 2
Author_xml – sequence: 1
  givenname: Yoshiaki
  surname: Kamada
  fullname: Kamada, Yoshiaki
  email: yoshikam@nibb.ac.jp, yohsumi@iri.titech.ac.jp
  organization: Division of Molecular Cell Biology, National Institute for Basic Biology
– sequence: 2
  givenname: Ken-ichi
  surname: Yoshino
  fullname: Yoshino, Ken-ichi
  organization: Biosignal Research Center, Kobe University
– sequence: 3
  givenname: Chika
  surname: Kondo
  fullname: Kondo, Chika
  organization: Division of Molecular Cell Biology, National Institute for Basic Biology
– sequence: 4
  givenname: Tomoko
  surname: Kawamata
  fullname: Kawamata, Tomoko
  organization: Division of Molecular Cell Biology, National Institute for Basic Biology
– sequence: 5
  givenname: Noriko
  surname: Oshiro
  fullname: Oshiro, Noriko
  organization: Biosignal Research Center, Kobe University
– sequence: 6
  givenname: Kazuyoshi
  surname: Yonezawa
  fullname: Yonezawa, Kazuyoshi
  organization: Biosignal Research Center, Kobe University
– sequence: 7
  givenname: Yoshinori
  surname: Ohsumi
  fullname: Ohsumi, Yoshinori
  email: yoshikam@nibb.ac.jp, yohsumi@iri.titech.ac.jp
  organization: Division of Molecular Cell Biology, National Institute for Basic Biology
BackLink https://www.ncbi.nlm.nih.gov/pubmed/19995911$$D View this record in MEDLINE/PubMed
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Snippet Article Usage Stats Services MCB Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley...
Autophagy is a bulk proteolytic process that is indispensable for cell survival during starvation. Autophagy is induced by nutrient deprivation via...
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StartPage 1049
SubjectTerms Amino Acid Sequence
Autophagy
Autophagy-Related Proteins
Microscopy, Electron
Molecular Sequence Data
Phosphorylation
Protein Binding
Protein Kinases - chemistry
Protein Kinases - genetics
Protein Kinases - metabolism
Protein-Serine-Threonine Kinases - genetics
Protein-Serine-Threonine Kinases - metabolism
Saccharomyces cerevisiae - cytology
Saccharomyces cerevisiae - enzymology
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae Proteins - chemistry
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - metabolism
Title Tor Directly Controls the Atg1 Kinase Complex To Regulate Autophagy
URI http://mcb.asm.org/content/30/4/1049.abstract
https://www.tandfonline.com/doi/abs/10.1128/MCB.01344-09
https://www.ncbi.nlm.nih.gov/pubmed/19995911
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Volume 30
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