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Rem inhibits skeletal muscle EC coupling by reducing the number of functional L-type Ca2+ channels

R A Bannister1, H M Colecraft, K G Beam

  • 1Department of Physiology and Biophysics, University of Colorado-Denver, Aurora, Colorado 80045, USA .

Biophysical Journal
|January 15, 2008
PubMed

Insights

Rem protein impairs skeletal muscle excitation-contraction (EC) coupling by reducing functional L-type Ca(2+) channels. This protein negatively regulates EC coupling by decreasing L-type Ca(2+) channel number in the plasma membrane.

Area of Science:

  • Molecular Biology
  • Cell Physiology
  • Muscle Biology

Background:

  • Skeletal muscle excitation-contraction (EC) coupling relies on L-type voltage-gated Ca(2+) channels.
  • RGK family proteins, including Rem, are known regulators of ion channel function.

Purpose of the Study:

  • To investigate the effect of Rem on skeletal muscle L-type Ca(2+) channel function and EC coupling.
  • To determine the mechanism by which Rem influences EC coupling.

Main Methods:

  • Expression of YFP-tagged Rem in myotubes.
  • Assay of EC coupling via electrically evoked contractions and myoplasmic Ca(2+) transients.
  • Assessment of ryanodine receptor function and Ca(2+) stores.
  • Measurement of L-type Ca(2+) current and membrane-bound charge movements.

Main Results:

  • Rem expression weakened EC coupling in myotubes.
  • Rem did not alter ryanodine receptor function or Ca(2+) stores.
  • Rem significantly reduced L-type Ca(2+) current (approx. 75%) and membrane charge movements.

Conclusions:

  • Rem negatively regulates skeletal muscle EC coupling.
  • Rem reduces the number of functional L-type Ca(2+) channels at the plasma membrane.

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