Structure-function analysis of inositol hexakisphosphate-induced autoprocessing in Clostridium difficile toxin A

J Biol Chem. 2009 Aug 14;284(33):21934-21940. doi: 10.1074/jbc.M109.018929. Epub 2009 Jun 24.

Abstract

The action of Clostridium difficile toxins A and B depends on inactivation of host small G-proteins by glucosylation. Cellular inositol hexakisphosphate (InsP6) induces an autocatalytic cleavage of the toxins, releasing an N-terminal glucosyltransferase domain into the host cell cytosol. We have defined the cysteine protease domain (CPD) responsible for autoprocessing within toxin A (TcdA) and report the 1.6 A x-ray crystal structure of the domain bound to InsP6. InsP6 is bound in a highly basic pocket that is separated from an unusual active site by a beta-flap structure. Functional studies confirm an intramolecular mechanism of cleavage and highlight specific residues required for InsP6-induced TcdA processing. Analysis of the structural and functional data in the context of sequences from similar and diverse origins highlights a C-terminal extension and a pi-cation interaction within the beta-flap that appear to be unique among the large clostridial cytotoxins.

Publication types

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

MeSH terms

  • Bacterial Toxins / chemistry*
  • Catalytic Domain
  • Cations
  • Clostridioides difficile / metabolism*
  • Crystallography, X-Ray / methods
  • Enterotoxins / chemistry*
  • Magnetic Resonance Spectroscopy
  • Models, Biological
  • Models, Molecular
  • Molecular Conformation
  • Phytic Acid / pharmacology*
  • Point Mutation
  • Protein Structure, Secondary
  • Protein Structure, Tertiary
  • Spectrophotometry / methods
  • Time Factors

Substances

  • Bacterial Toxins
  • Cations
  • Enterotoxins
  • tcdA protein, Clostridium difficile
  • Phytic Acid

Associated data

  • PDB/3HO6