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Cardiac actin changes in the actomyosin interface have different effects on myosin duty ratio

Haidun Liu1,1, Mary Henein1,1, Maria Anillo1,1

  • 1Department of Molecular and Cellular Biology and the Centre for Cardiovascular Investigations, University of Guelph, Guelph, ON N1G 2W1, Canada.

Biochemistry and Cell Biology = Biochimie Et Biologie Cellulaire
|October 4, 2017
PubMed

Insights

Hypertrophic cardiomyopathy (HCM) linked actin variants do not alter myosin duty ratio, suggesting other factors contribute to this inherited heart disease. Further research is needed to understand HCM development.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Inherited Cardiovascular Diseases

Background:

  • Hypertrophic cardiomyopathy (HCM) is an inherited cardiovascular disease characterized by left ventricular hypertrophy.
  • Cardiac muscle contraction involves the actomyosin ATPase cycle, with myosin's duty ratio (r) being crucial for force generation.
  • A prevailing hypothesis suggests HCM-associated mutations enhance cardiac sarcomere contraction, but evidence remains inconclusive.

Purpose of the Study:

  • To investigate whether human α-cardiac actin (ACTC) variants linked to HCM alter myosin's duty ratio (r).
  • To test the hypothesis that ACTC variants near the myosin binding site increase myosin binding to actin, thereby increasing force production.

Main Methods:

  • Calculated myosin duty ratios (r) using human ACTC variant proteins.
  • Assessed myosin ATPase activity and in-vitro motility assays to determine r.
  • Utilized established biochemical and biophysical techniques for protein analysis.

Main Results:

  • No consistent alterations in the duty ratio (r) were observed for the studied ACTC variants.
  • Myosin's interaction with HCM-linked ACTC variants did not significantly change under experimental conditions.
  • The findings do not support the hypothesis that increased myosin duty ratio is a primary mechanism in HCM caused by these ACTC variants.

Conclusions:

  • The duty ratio of myosin is not consistently affected by HCM-linked ACTC variants near the myosin binding site.
  • These findings suggest that other molecular or cellular factors, beyond altered myosin duty ratio, likely contribute to the pathogenesis of HCM in the presence of ACTC variants.
  • Further investigation is warranted to elucidate the complete mechanisms underlying HCM development.

Keywords:
actine cardiaqueactomyosinactomyosinecardiac actincardiomyopathie hypertrophiqueduty ratiofacteur de marchehypertrophic cardiomyopathymutations

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