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Protons act as a transmitter for muscle contraction in C. elegans.

Muscle contraction is normally mediated by the release of neurotransmitters from motor neurons. Here we demonstrate that protons can act as a direct transmitter from intestinal cells to stimulate muscle contraction. During the C. elegans defecation motor program the posterior body muscles contract even in the absence of neuronal inputs or vesicular neurotransmission. In this study, we demonstrate that the space between the intestine and the muscle is acidified just prior to muscle contraction and that the release of caged protons is sufficient to induce muscle contraction. PBO-4 is a putative Na+/H+ ion exchanger expressed on the basolateral membrane of the intestine, juxtaposed to the posterior body muscles. In pbo-4 mutants the extracellular space is not acidified and the muscles fail to contract. The pbo-5 and pbo-6 genes encode subunits of a "cys-loop" proton-gated cation channel required for muscles to respond to acidification. In heterologous expression assays the PBO receptor is half-maximally activated at a pH of 6.8. The identification of the mechanisms for release and reception of proton signals establishes a highly unusual mechanism for intercellular communication.

Pubmed ID: 18191228

Authors

  • Beg AA
  • Ernstrom GG
  • Nix P
  • Davis MW
  • Jorgensen EM

Journal

Cell

Publication Data

January 11, 2008

Associated Grants

  • Agency: NINDS NIH HHS, Id: R37 NS034307
  • Agency: NINDS NIH HHS, Id: R37 NS034307-13
  • Agency: Howard Hughes Medical Institute, Id:

Mesh Terms

  • Animals
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Cell Communication
  • Cell Membrane
  • Defecation
  • Intestines
  • Ion Channel Gating
  • Ion Channels
  • Muscle Contraction
  • Muscles
  • Protein Subunits
  • Protons
  • Signal Transduction
  • Sodium-Hydrogen Antiporter