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N-terminal acetylation regulates autophagy.

Lan Jiang1, Tianyun Shen1, Xinyuan Wang2

  • 1Department of Pathology, West China Second University Hospital, State Key Laboratory of Biotherapy, and Key Laboratory of Birth Defects and Related Diseases of Women and Children of Ministry of Education, Sichuan University, Chengdu, China.

Autophagy
|January 29, 2022
PubMed
Summary

N-terminal acetylation by NatB is crucial for autophagy. NatB targets proteins like Act1 and Vps1, but other substrates are also involved in regulating this vital cellular process.

Keywords:
Atg9N-terminal acetylationNATBSNARE complexautophagosomeautophagycytoskeletonfusion

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Biochemistry

Background:

  • Posttranslational modifications regulate protein function, with N-terminal acetylation being less understood than lysine acetylation.
  • Macroautophagy/autophagy is essential for cellular homeostasis, and its regulation is a key area of research.

Purpose of the Study:

  • To investigate the role of N-terminal acetylation in autophagy.
  • To identify substrates of the N-terminal acetyltransferase NatB involved in autophagy.

Main Methods:

  • Genetic deletion of NatB complex components.
  • Identification and analysis of NatB substrates (Act1, Vps1).
  • Assessment of autophagosome formation and fusion defects.

Main Results:

  • NatB is essential for autophagy, and its deficiency blocks autophagosome formation.
  • NatB acetylates Act1, promoting actin filament formation and vesicle trafficking.
  • NatB acetylates Vps1, enhancing SNARE interactions and autophagosome-vacuole fusion.
  • Restoring Act1 and Vps1 acetylation does not rescue autophagy in NatB-deficient cells.

Conclusions:

  • N-terminal acetylation by NatB is critical for multiple steps in autophagy.
  • Act1 and Vps1 are key substrates, but additional NatB targets are involved in autophagy regulation.