S-acylation regulates SQSTM1/p62-mediated selective autophagy

Autophagy. 2024 Jun;20(6):1467-1469. doi: 10.1080/15548627.2023.2297623. Epub 2024 Jan 1.

Abstract

Macroautophagy/autophagy is a highly conserved metabolic process that degrades intracellular components and recycles bioenergetic substrates. SQSTM1/p62 (sequestosome 1) is a classical autophagy receptor that participates in selective autophagy to eliminate abnormal intracellular components and recycle bioenergetic substrates. In autophagy, SQSTM1 recruits ubiquitinated substrates to form SQSTM1 droplets and delivers these cargoes to phagophores, the precursors to autophagosomes. Recently, we reported a previously unidentified SQSTM1 S-acylation, which is catalyzed by S-acyltransferase ZDHHC19 and reversed by LYPLA1/APT1. S-acylation of SQSTM1 enhances the affinity of SQSTM1 droplets with the phagophore membrane, thereby promoting efficient autophagic degradation of ubiquitinated substrates. Our study uncovers the role of the S-acylation-deacylation cycle in regulating SQSTM1-mediated selective autophagy.

Keywords: Autophagosome; LYPLA1/APT1; S-acylation; SQSTM1; ZDHHC19; selective autophagy.

MeSH terms

  • Acylation
  • Animals
  • Autophagosomes / metabolism
  • Autophagy* / physiology
  • Humans
  • Sequestosome-1 Protein* / metabolism

Substances

  • Sequestosome-1 Protein
  • SQSTM1 protein, human

Grants and funding

This study was supported by the National Natural Science Foundation of China (NSFC) (32170185, 91854101, 31801166 and 22011530161), the Natural Science Foundation of Chongqing, China [CSTB2022NSCQ-MSX0463], the Venture and Innovation Support Program for Chongqing Overseas Returnees grant cx2022066, and the Fundamental Research Funds for the Central Universities [2022CDJYGRH-002].