Finally, removal of Ca from troponin restores the blocking position of , the cro
ID: 3477379 • Letter: F
Question
Finally, removal of Ca from troponin restores the blocking position of , the cross-bridge cycling ceases, and the skeletal muscle fiber actin cross-bridges Ca2-ATPases Cross-bridge binding triggers the release of ATP hydrolysis products from and produces the , which generates force ryanodine receptors power stroke Cytosolic Ca* decreases as the actively transport Ca2 back into tropomyosin hydrolyzed Ca2 binds to move away from its blocking position, thereby uncovering cross-bridge binding sites on on the thin filaments, causing tropomyosin to contracts myosin These channels are embedded within the membrane of the sarcoplasmic reticulum, and when they are open, they allow the release of from the relaxes terminal dissociate troponin binds to myosin, breaking the linkage between actin and myosin and thereby allowing the cross-bridges to from actin dihydropyridine receptors ATP Energized portions of myosin molecules called bind to actin sarcoplasmic reticulum , energizing the cross-bridge, and ATP bound to myosin is another round of cross-bridge cycling occurs as long as Ca2 remains bound to troponin Action potentials that propagate along the T-tubules induce membrane proteins called to pull open channels that are calledExplanation / Answer
1. Finally, removal of calcium from troponin restores the blocking position of tropomyosin, the cross bridge recycling ceases, and the skeletal muscle fiber relaxes.
2 .Cross bridge binding triggers the release of ATP hydrolysis products from myosin and produces the power-stroke which generates force.
3. Calcium binds to troponin on the thin filaments, causing trophomyosin to move away from its blocking position, thereby uncovering cross-bridging sites on actin.
4. These channels are embedded within the membrane of the sarcoplasmic reticulum, and when they are open allow the release of Ca2+ from the terminal cisternae.
5. ATP binds to myosin, breaking the linkage between actin and myosin, thereby allowing the cross-bridge to dissociate from actin.
6. Energised portions of myosin molecules called cross bridges bind to actin.
7. ATP bound to myosin is hydrolyzed, energizing the crossbridge and another round of cross-bridge cycling occurs as long as Ca2+ is bound to troponin.
8. Action potentials that propagate along the t tubules include membrane proteins called dihydropyridine receptors to pull open channels called ryanodine receptors.
Mechanism:
The contraction of skeletal muscle is triggered by nerve impulses. These impulses stimulate the release of Ca2+ from the sarcoplasmic reticulum. Calcium is stored in terminal cisternae present in the muscle cell.
The action potential generated across the membrane travels to middle of the muscle fiber, inducing depolarization.- Depolarization of the T-tubule membrane activates dihydropyridine receptors. These receptor bind to ryanodine receptors to open and release calcium from its stores.
Muscle contraction is initiated when tropomyosin exposes myosin-binding site on an actin filament. This allows cross-bridging between the actin and myosin microfilaments. Binding of ATP to myosin dissociates the myosin-actin complex. ATP is hydrolyzed that induces a conformational change in myosin. ADP and Pi remain bound to myosin
Myosin releases the ADP and Pi generated from ATP, when it binds to new actin, triggering the power stroke in which myosin returns to its original confirmation, sliding actin filaments to the M line of the sarcomere.
When ca2+ levels falls, tropomyosin interaction is reinstated and the muscle relaxes.
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