Apratoxin Kills Cells by Direct Blockade of the Sec61 Protein Translocation Channel

Cell Chem Biol. 2016 May 19;23(5):561-566. doi: 10.1016/j.chembiol.2016.04.008.

Abstract

Apratoxin A is a cytotoxic natural product that prevents the biogenesis of secretory and membrane proteins. Biochemically, apratoxin A inhibits cotranslational translocation into the ER, but its cellular target and mechanism of action have remained controversial. Here, we demonstrate that apratoxin A prevents protein translocation by directly targeting Sec61α, the central subunit of the protein translocation channel. Mutagenesis and competitive photo-crosslinking studies indicate that apratoxin A binds to the Sec61 lateral gate in a manner that differs from cotransin, a substrate-selective Sec61 inhibitor. In contrast to cotransin, apratoxin A does not exhibit a substrate-selective inhibitory mechanism, but blocks ER translocation of all tested Sec61 clients with similar potency. Our results suggest that multiple structurally unrelated natural products have evolved to target overlapping but non-identical binding sites on Sec61, thereby producing distinct biological outcomes.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Death / drug effects
  • Depsipeptides / chemistry
  • Depsipeptides / pharmacology*
  • Dose-Response Relationship, Drug
  • HCT116 Cells
  • Humans
  • Molecular Structure
  • Protein Transport / drug effects
  • SEC Translocation Channels / antagonists & inhibitors*
  • SEC Translocation Channels / metabolism
  • Structure-Activity Relationship

Substances

  • Depsipeptides
  • SEC Translocation Channels
  • SEC61A1 protein, human
  • apratoxin A