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Effects of cardiac Myosin binding protein-C on actin motility are explained with a drag-activation-competition model

Sam Walcott1, Steffen Docken1, Samantha P Harris2

  • 1Department of Mathematics, University of California at Davis, Davis, California.

Biophysical Journal
|January 8, 2015
PubMed

Insights

Cardiac myosin binding protein-C (cMyBP-C) mutations cause heart disease. A new mathematical model reveals a drag-activation-competition mechanism explains cMyBP-C’s complex effects on muscle contraction.

Area of Science:

  • Muscle physiology
  • Biophysics
  • Cardiovascular research

Background:

  • Mutations in cardiac myosin binding protein-C (cMyBP-C) are linked to heart disease.
  • The precise molecular mechanisms underlying cMyBP-C's function in muscle contraction remain unclear.
  • Observed dual effects (activation/inhibition) in assays complicate understanding.

Purpose of the Study:

  • To elucidate the mechanism of cardiac myosin binding protein-C (cMyBP-C) in muscle contraction.
  • To explain the complex, biphasic effects of cMyBP-C observed in actin motility assays.
  • To develop a predictive mathematical model for cMyBP-C interactions.

Main Methods:

  • Developed a mathematical model simulating interactions between cMyBP-C, actin, myosin, and tropomyosin.
  • Utilized actin motility assays to test model predictions.
  • Compared model performance with and without drag and competition components.

Main Results:

  • A drag-activation-competition mechanism accurately describes actin motility data.
  • Models excluding either drag or competition failed to replicate experimental observations.
  • The study demonstrates that cMyBP-C's complex effects can stem from simple actin binding.

Conclusions:

  • The drag-activation-competition mechanism provides a unified explanation for cMyBP-C's functional effects.
  • This model advances our understanding of cardiac muscle contractility regulation.
  • Findings highlight the importance of considering multiple interaction components in protein function.

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