myosin

Examples of myosin in the following topics:

• Rigor Mortis

  • Physiologically, rigor mortis is caused a release of calcium facilitating crossbridges in the sarcomeres; the coupling between myosin and actin cannot be broken, creating a constant state of muscle contraction until enzymatic decomposition eventually removes the crossbridges.
  • Diffusion of the calcium through the pumps occurs, facilitation binding of myosin and actin filaments.
  • As part of the process of decomposition, the myosin heads are degraded by the enzymes, allowing the muscle contraction to release and the body to relax.
  • Diagram showing Actin-Myosin filaments in Smooth muscle.
  • When activated they slide over the myosin bundles causing shortening of the cell walls.

• Microscopic Anatomy

  • The two most important proteins within sarcomeres are myosin, which forms a thick, flexible filament, and actin, which forms the thin, more rigid filament.
  • Myosin has a long, fibrous tail and a globular head, which binds to actin.
  • The myosin head also binds to ATP, which is the source of energy for muscle movement.
  • Together, myosin and actin form myofibrils, the repeating molecular structure of sarcomeres.
  • When ATP binds to myosin, it seperates from the actin of the myofibril, which causes a contraction.

• Mechanism and Contraction Events of Cardiac Muscle Fibers

  • In the sliding filament model, myosin filaments slide along actin filaments to shorten or lengthen the muscle fiber for contraction and relaxation.
  • This removal of the troponin complex frees the actin to be bound by myosin and initiates contraction.
  • The myosin head binds to ATP and pulls the actin filaments toward the center of the sarcomere, contracting the muscle.
  • This animation shows myosin filaments (red) sliding along the actin filaments (pink) to contract a muscle cell.

• Short-Term Chemical Control

  • The mechanism that leads to vasoconstriction results from the increased concentration of calcium (Ca2+ ions) and phosphorylated myosin within vascular smooth muscle cells.
  • The rise in intracellular calcium complexes with calmodulin, which in turn activates myosin light chain kinase.
  • This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross bridge cycling.
  • As with vasoconstriction vasodilation is modulated by calcium ion concentration and myosin phosphorylation within vascular smooth muscle cells.
  • Dephosphorylation by myosin light-chain phosphatase and induction of calcium symportersand antiporters that pump calcium ions out of the intracellular compartment both contribute to smooth muscle cell relaxation and therefore vasodilation.

• Overview of Motor Integration

• Force of Muscle Contraction

  • When a sarcomere contracts, myosin heads attach to actin to form cross-bridges.
  • Simply put,  the tension generated in skeletal muscle is a function of the magnitude of overlap between actin and myosin myofilaments.
  • The force generated by a muscle depends on the number of actin and myosin cross-bridges formed; a larger number of cross-bridges results in a larger amount of force.

• Myocardial Thickness and Function

  • Two of the important proteins found in sarcomeres are myosin, which forms the thick filament, and actin, which forms the thin filament.
  • Myosin has a long, fibrous tail and a globular head, which binds to actin.
  • The myosin head also binds to ATP, which is the source of energy for cellular metabolism, and is required for the cardiomyocytes to sustain themselves and function normally.
  • Together, myosin and actin form myofibril filaments, which are the elongated, contractile threads found in muscle tissue.

• Velocity and Duration of Muscle Contraction

  • The force generated by a muscle depends on the number of actin and myosin cross-bridges formed; a larger number of cross-bridges results in a larger amount of force.

• Myocarditis and Endocarditis

  • Streptococcal M protein and coxsackievirus B have regions (epitopes) that are immunologically similar to cardiac myosin.
  • After the virus is gone, the immune system may attack cardiac myosin.

• Exercise-Induced Muscle Damage

  • Delayed onset muscle soreness is caused by structural damage to the Z disk and myosin and actin filaments.