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CERKL regulates autophagy via the NAD-dependent deacetylase SIRT1

Xuebin Hu1, Zhaojing Lu1, Shanshan Yu1

  • 1a Key Laboratory of Molecular Biophysics of Ministry of Education, Department of Genetics and Developmental Biology , College of Life Science and Technology, Huazhong University of Science and Technology , Wuhan , Hubei , P.R. China.

Autophagy
|September 13, 2018
PubMed

Insights

The ceramide kinase like (CERKL) gene stabilizes SIRT1, a key regulator of autophagy. Suppressing CERKL impairs autophagy by downregulating SIRT1 and increasing acetylation of essential autophagy proteins.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Macroautophagy (autophagy) is crucial for cellular homeostasis.
  • CERKL is a gene linked to retinal degeneration (RD).
  • SIRT1 is a key regulator of acetylation/deacetylation in autophagy.

Purpose of the Study:

  • To investigate the role of CERKL in regulating autophagy.
  • To elucidate the mechanism by which CERKL influences autophagy.
  • To determine the relationship between CERKL, SIRT1, and autophagy.

Main Methods:

  • In vitro and in vivo experiments.
  • Gene suppression and overexpression studies.
  • Analysis of protein acetylation and phosphorylation.
  • Protein-protein interaction studies.

Main Results:

  • CERKL suppression impairs autophagy and downregulates SIRT1.
  • CERKL depletion increases acetylation of ATG5 and ATG7.
  • SIRT1 overexpression rescues autophagy in CERKL-depleted cells.
  • CERKL interacts with SIRT1 and may regulate its phosphorylation at Ser27 to stabilize it.

Conclusions:

  • CERKL is a critical regulator of autophagy.
  • CERKL stabilizes SIRT1, thereby promoting autophagy.
  • The CERKL-SIRT1 interaction is essential for autophagy regulation.
Keywords:
AutophagyCERKLSIRT1deacetylationretinitis pigmentosastabilization

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