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Calcium transients regulate patterned actin assembly during myofibrillogenesis.

Hongyan Li1, John D Cook, Monica Terry

  • 1Department of Biological Sciences, University of Arkansas, Fayetteville, Arkansas, USA.

Developmental Dynamics : an Official Publication of the American Association of Anatomists
|January 28, 2004
PubMed
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Spontaneous calcium (Ca2+) transients are crucial for ordered sarcomeric myosin assembly during muscle development. Disrupting these transients or actin dynamics significantly impacts myosin organization, highlighting calcium

Area of Science:

  • Muscle Development
  • Sarcomere Assembly
  • Calcium Signaling

Background:

  • Striated muscle development relies on the precise, ordered arrangement of sarcomeric myosin.
  • Spontaneous calcium (Ca2+) transients are known to be essential for this highly ordered myosin assembly.
  • The temporal assembly patterns of various sarcomeric proteins, including actin, titin, and capZ, are conserved.

Purpose of the Study:

  • To investigate the role of spontaneous calcium (Ca2+) transients in the patterned assembly of sarcomeric proteins.
  • To determine the relative temporal interdependencies between thick (myosin) and thin (actin) filament formation during sarcomere assembly.
  • To elucidate the sensitivity of myosin thick filament assembly to disruptions in actin and titin filament systems.

Main Methods:

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  • Utilized selective inhibitors to disrupt thick filament (myosin light chain kinase inhibitors like ML-7, PMA) and thin filament (actin dynamics inhibitors like cytochalasin D) formation.
  • Observed the effects of these inhibitors on the patterned assembly of actin, titin, capZ, and myosin.
  • Analyzed the temporal interdependencies of protein assembly by assessing the impact of inhibiting specific components.

Main Results:

  • Blocking spontaneous calcium (Ca2+) transients compromised the patterned assembly of actin, titin, and capZ, in addition to myosin.
  • Inhibition of myosin light chain kinase (MLCK) primarily disrupted myosin assembly, with minimal effect on actin bands.
  • While actin dynamics inhibitors (cytochalasin D) caused minor disruptions to actin, titin, and capZ, they significantly perturbed myosin organization.

Conclusions:

  • Calcium (Ca2+) transients regulate early steps in sarcomere formation.
  • Mature actin filaments can assemble independently of myosin band formation.
  • Myosin thick filament assembly is highly sensitive to disruptions in either the actin or titin filament systems.