Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
Regulated Protein Degradation02:58

Regulated Protein Degradation

It is vital to regulate the activity of enzymatic as well as non-enzymatic proteins inside the cell. This can be achieved either through creating a balance between their rate of synthesis and degradation or regulating the intrinsic activity of the protein. Both these regulation mechanisms play an essential role in the normal functioning of cells.
Protein degradation plays two important roles in the cells. It helps to protect cells from misfolded or damaged proteins before they lead to a...
Regulated Protein Degradation02:58

Regulated Protein Degradation

It is vital to regulate the activity of enzymatic as well as non-enzymatic proteins inside the cell. This can be achieved either through creating a balance between their rate of synthesis and degradation or regulating the intrinsic activity of the protein. Both these regulation mechanisms play an essential role in the normal functioning of cells.
Protein degradation plays two important roles in the cells. It helps to protect cells from misfolded or damaged proteins before they lead to a...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Association between Phosphate Binders and Constipation in Patients Undergoing Chronic Hemodialysis: A Cross-sectional Study.

Internal medicine (Tokyo, Japan)·2025
Same author

Impact of maximal overexpression of a non-toxic protein on yeast cell physiology.

eLife·2025
Same author

DHX8 regulates degradation of RNA by RNautophagy.

Nucleic acids research·2025
Same author

High Serum Ferritin Levels Are Associated with Sarcopenia in Patients Undergoing Chronic Hemodialysis.

Nutrients·2025
Same author

Efficacy of the PD-1 inhibitor penpulimab in combination with chemotherapy for advanced lung squamous cell carcinoma: insights from a phase III multicenter study.

Journal of thoracic disease·2025
Same author

Association between Serum Zinc Levels and Trabecular Bone Scores among Patients Undergoing Chronic Hemodialysis.

American journal of nephrology·2025

Related Experiment Video

Updated: Jun 17, 2026

Study of Protein-protein Interactions in Autophagy Research
14:08

Study of Protein-protein Interactions in Autophagy Research

Published on: September 9, 2017

Tor directly controls the Atg1 kinase complex to regulate autophagy.

Yoshiaki Kamada1, Ken-ichi Yoshino, Chika Kondo

  • 1Division of Molecular Cell Biology, National Institute for Basic Biology, Okazaki 444-8585, Japan. yoshikam@nibb.ac.jp

Molecular and Cellular Biology
|December 10, 2009
PubMed
Summary

Autophagy, essential for cell survival, is regulated by Tor complex1 (TORC1). This study reveals TORC1 directly phosphorylates Atg13, a key autophagy protein, controlling the process.

More Related Videos

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase
09:51

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase

Published on: June 30, 2023

Imaging ATG9A, a Multi-Spanning Membrane Protein
07:20

Imaging ATG9A, a Multi-Spanning Membrane Protein

Published on: June 16, 2023

Related Experiment Videos

Last Updated: Jun 17, 2026

Study of Protein-protein Interactions in Autophagy Research
14:08

Study of Protein-protein Interactions in Autophagy Research

Published on: September 9, 2017

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase
09:51

Cell-Based Drug Screening for Inhibitors of Autophagy Related 4B Cysteine Peptidase

Published on: June 30, 2023

Imaging ATG9A, a Multi-Spanning Membrane Protein
07:20

Imaging ATG9A, a Multi-Spanning Membrane Protein

Published on: June 16, 2023

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Autophagy is a crucial cellular degradation process vital for survival under starvation.
  • Nutrient deprivation induces autophagy by inactivating the Tor complex1 (TORC1), a key regulator of cell growth.
  • The precise mechanism of TORC1-mediated autophagy regulation and its direct targets are not fully understood.

Purpose of the Study:

  • To elucidate the mechanism by which TORC1 controls autophagy.
  • To identify the direct target of TORC1 activity in the autophagy pathway.
  • To investigate the role of Atg13 phosphorylation in TORC1-mediated autophagy.

Main Methods:

  • Investigated the interaction between TORC1 and Atg13 in yeast.
  • Utilized site-directed mutagenesis to create an unphosphorylatable Atg13 mutant.
  • Assessed autophagy induction and Atg1 activation under nutrient-rich conditions using the Atg13 mutant.

Main Results:

  • Demonstrated that yeast TORC1 directly phosphorylates Atg13 at multiple serine residues.
  • Showed that an Atg13 mutant, unable to be phosphorylated, bypasses TORC1 inhibition.
  • Observed that this unphosphorylatable Atg13 mutant induces autophagy and activates Atg1 even in nutrient-rich conditions.

Conclusions:

  • TORC1 directly regulates autophagy by phosphorylating Atg13, a component upstream of the Atg1 kinase complex.
  • Phosphorylation of Atg13 by TORC1 is a critical step in suppressing autophagy under nutrient-rich conditions.
  • Targeting Atg13 phosphorylation offers a potential mechanism for controlling autophagy induction.