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RyR1 modulation by oxidation and calmodulin.

S L Hamilton1, M B Reid

  • 1Department of Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, TX 77030, USA. susanh@bcm.tmc.edu

Antioxidants & Redox Signaling
|March 10, 2001
PubMed
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Reactive oxygen species and nitric oxide (NO) regulate skeletal muscle function by affecting the Ca2+ release channel (RyR1). NO and oxidants impact RyR1 activity and calmodulin binding, influencing muscle contraction.

Area of Science:

  • Biochemistry
  • Muscle Physiology
  • Cellular Signaling

Background:

  • Skeletal muscle function is modulated by reactive oxygen species (ROS) and nitric oxide (NO).
  • The skeletal muscle Ca2+ release channel, RyR1, is a key regulator of muscle contraction and its activity can be altered by ROS and NO.
  • Understanding these interactions is crucial for elucidating mechanisms of muscle function and dysfunction.

Purpose of the Study:

  • To investigate the regulatory roles of oxidants and nitric oxide (NO) on skeletal muscle Ca2+ release channel (RyR1) activity.
  • To determine how ROS and NO affect RyR1 inter-subunit crosslinking and calmodulin binding.
  • To elucidate the specific molecular mechanisms underlying RyR1 regulation by these signaling molecules.

Main Methods:

  • Utilized biochemical assays to assess RyR1 activation and inter-subunit disulfide bond formation.

Related Experiment Videos

  • Employed chemical modifications (N-ethylmaleimide) and NO donors to probe RyR1 sulfhydryl groups.
  • Investigated the binding kinetics of Ca2+-calmodulin and apocalmodulin to RyR1 under various oxidative conditions.

    • Main Results:

    • Oxidants activate RyR1 and promote inter-subunit disulfide bonds, effects inhibited by NO donors or N-ethylmaleimide.
    • Oxidation-induced crosslinking is prevented by Ca2+-calmodulin or apocalmodulin binding.
    • Oxidation blocks Ca2+-calmodulin and apocalmodulin binding, suggesting a regulatory cysteine (Cys3635) within the apocalmodulin-binding site.
    • NO and calmodulin binding sites overlap but are not identical; Cys3635 is involved in both disulfide bond formation and apocalmodulin binding.

    Conclusions:

    • Oxidants regulate RyR1 activity directly via subunit interactions and indirectly by inhibiting calmodulin binding.
    • NO exerts both direct and indirect regulatory effects on RyR1, blocking oxidant-induced crosslinking and apocalmodulin binding.
    • Findings suggest a model where NO and oxidative stress modulate skeletal muscle function through intricate regulation of RyR1 structure and calmodulin interaction.