Structural basis for tetrodotoxin-resistant sodium channel binding by mu-conotoxin SmIIIA

J Biol Chem. 2003 Nov 21;278(47):46805-13. doi: 10.1074/jbc.M309222200. Epub 2003 Sep 10.

Abstract

SmIIIA is a new micro-conotoxin isolated recently from Conus stercusmuscarum. Although it shares several biochemical characteristics with other micro-conotoxins (the arrangement of cysteine residues and a conserved arginine believed to interact with residues near the channel pore), it has several distinctive features, including the absence of hydroxyproline, and is the first specific antagonist of tetrodotoxin-resistant voltage-gated sodium channels to be characterized. It therefore represents a potentially useful tool to investigate the functional roles of these channels. We have determined the three-dimensional structure of SmIIIA in aqueous solution. Consistent with the absence of hydroxyprolines, SmIIIA adopts a single conformation with all peptide bonds in the trans configuration. The spatial orientations of several conserved Arg and Lys side chains, including Arg14 (using a consensus numbering system), which plays a key role in sodium channel binding, are similar to those in other micro-conotoxins but the N-terminal regions differ, reflecting the trans conformation for the peptide bond preceding residue 8 in SmIIIA, as opposed to the cis conformation in micro-conotoxins GIIIA and GIIIB. Comparison of the surfaces of SmIIIA with other micro-conotoxins suggests that the affinity of SmIIIA for TTX-resistant channels is influenced by the Trp15 side chain, which is unique to SmIIIA. Arg17, which replaces Lys in the other micro-conotoxins, may also be important. Consistent with these inferences from the structure, assays of two chimeras of SmIIIA and PIIIA in which their N- and C-terminal halves were recombined, indicated that residues in the C-terminal half of SmIIIA confer affinity for tetrodotoxin-resistant sodium channels in the cell bodies of frog sympathetic neurons. SmIIIA and the chimera possessing the C-terminal half of SmIIIA also inhibit tetrodotoxin-resistant sodium channels in the postganglionic axons of sympathetic neurons, as indicated by their inhibition of C-neuron compound action potentials that persist in the presence of tetrodotoxin.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / drug effects
  • Amino Acid Sequence
  • Animals
  • Axons / chemistry
  • Conotoxins / chemistry*
  • Conotoxins / metabolism
  • Conotoxins / pharmacology
  • Mollusk Venoms / chemistry
  • Mollusk Venoms / metabolism
  • Mollusk Venoms / pharmacology
  • Neuropeptides / antagonists & inhibitors
  • Neuropeptides / chemistry*
  • Neuropeptides / metabolism
  • Protein Binding
  • Protein Conformation
  • Ranidae
  • Recombinant Fusion Proteins
  • Snails
  • Sodium Channels / chemistry*
  • Sodium Channels / metabolism
  • Structure-Activity Relationship

Substances

  • Conotoxins
  • Mollusk Venoms
  • Neuropeptides
  • Recombinant Fusion Proteins
  • Sodium Channels