Phospho-regulation and function of ULK1-ATG13 during the cell cycle

Related Experiment Video

Updated: Nov 15, 2025

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
12:26

Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

19.1K

Zhiyuan Li1,2, Xin Zhang1,3

  • 1High Magnetic Field Laboratory, Key Laboratory of High Magnetic Field and Ion Beam Physical Biology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei, P. R. China.

Autophagy
|March 5, 2021
PubMed

Insights

The ULK1-ATG13 autophagy complex regulates cell cycle progression. CDK1-CCNB/cyclin B phosphorylation of ULK1-ATG13 promotes mitotic autophagy and cell division, impacting tumor growth.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The interplay between autophagy and the cell cycle is complex, with some autophagy-related proteins known to influence cell division.
  • The specific role of the ULK1-ATG13 complex, a core component of macroautophagy, in cell cycle regulation remained largely undefined.

Purpose of the Study:

  • To elucidate the function of the ULK1-ATG13 complex in cell cycle regulation.
  • To investigate the relationship between ULK1-ATG13 phosphorylation and cell cycle progression.
  • To determine the impact of ULK1-ATG13 on tumor cell proliferation.

Main Methods:

  • Investigated ULK1 and ATG13 as substrates of CDK1-CCNB/cyclin B.
  • Analyzed the effect of CDK1-induced phosphorylation on ULK1-ATG13 activity.
  • Performed ULK1 and ATG13 double-knockout experiments in vitro and in vivo.
  • Assessed the impact on cell cycle progression and tumor cell proliferation.

Main Results:

  • Mitotic ULK1 and ATG13 were identified as substrates of the cell cycle regulator CDK1-CCNB/cyclin B.
  • CDK1-induced phosphorylation of ULK1-ATG13 was found to promote both mitotic autophagy and cell cycle progression.
  • Simultaneous knockout of ULK1 and ATG13 significantly impaired cell cycle progression and tumor cell proliferation both in vitro and in vivo.

Conclusions:

  • Established a link between autophagic kinases (ULK1-ATG13) and mitotic kinases (CDK1-CCNB), revealing mutual regulation.
  • Demonstrated that ULK1-ATG13 phosphorylation is crucial for mitotic autophagy and cell cycle advancement.
  • Provided a mechanistic basis for targeting autophagy and cell division in combination therapies for related diseases.
Keywords:
ATG13CDK1ULK1autophagymitosis

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