Identification and characterisation of the RalA-ERp57 interaction: evidence for GDI activity of ERp57

PLoS One. 2012;7(11):e50879. doi: 10.1371/journal.pone.0050879. Epub 2012 Nov 30.

Abstract

RalA is a membrane-associated small GTPase that regulates vesicle trafficking. Here we identify a specific interaction between RalA and ERp57, an oxidoreductase and signalling protein. ERp57 bound specifically to the GDP-bound form of RalA, but not the GTP-bound form, and inhibited the dissociation of GDP from RalA in vitro. These activities were inhibited by reducing agents, but no disulphide bonds were detected between RalA and ERp57. Mutation of all four of ERp57's active site cysteine residues blocked sensitivity to reducing agents, suggesting that redox-dependent conformational changes in ERp57 affect binding to RalA. Mutations in the switch II region of the GTPase domain of RalA specifically reduced or abolished binding to ERp57, but did not block GTP-specific binding to known RalA effectors, the exocyst and RalBP1. Oxidative treatment of A431 cells with H(2)O(2) inhibited cellular RalA activity, and the effect was exacerbated by expression of recombinant ERp57. The oxidative treatment significantly increased the amount of RalA localised to the cytosol. These findings suggest that ERp57 regulates RalA signalling by acting as a redox-sensitive guanine-nucleotide dissociation inhibitor (RalGDI).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cell Line
  • Guanine Nucleotide Dissociation Inhibitors / metabolism*
  • Guanosine Diphosphate / metabolism
  • Humans
  • Molecular Sequence Data
  • Oxidation-Reduction
  • Oxidative Stress
  • Peptides / chemistry
  • Protein Binding
  • Protein Disulfide-Isomerases / chemistry
  • Protein Disulfide-Isomerases / metabolism*
  • Rats
  • Subcellular Fractions / metabolism
  • ral GTP-Binding Proteins / metabolism*

Substances

  • Guanine Nucleotide Dissociation Inhibitors
  • Peptides
  • Guanosine Diphosphate
  • ral GTP-Binding Proteins
  • PDIA3 protein, rat
  • Protein Disulfide-Isomerases
  • PDIA3 protein, human

Grants and funding

This work was supported by grants from the Australian National Health and Medical Research Council (NHMRC). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.