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question 5 (1.25 points)
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for the sliding filament model to work,
- acetylcholine is released and the sarcomere shortens
- tropomyosin breaks down to troponin, resulting in muscle contraction
- atp is produced and it binds to actin
- ca²+ binds to troponin, resulting in shifting of tropomyosin
- ca²+ binds to tropomyosin, and the sarcomere relaxes
Brief Explanations
- In the sliding filament model:
- Acetylcholine release is the start of muscle contraction signaling but alone doesn't directly make the sarcomere shorten in the context of the sliding mechanism details.
- Tropomyosin doesn't break down to troponin. They are different regulatory proteins.
- ATP binds to myosin, not actin, for the cross - bridge cycle.
- When \(Ca^{2+}\) binds to troponin, it causes a conformational change that shifts tropomyosin, uncovering the myosin - binding sites on actin, which is crucial for the sliding of filaments (actin and myosin) in muscle contraction.
- \(Ca^{2+}\) binding to tropomyosin is not the correct regulatory step for the sliding filament model (it binds to troponin), and when \(Ca^{2+}\) is removed (not when binding in the wrong way), the sarcomere relaxes.
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- \(Ca^{2+}\) binds to troponin, resulting in shifting of tropomyosin