Name that anatomy
This protein is found in the thin filament and provides the binding site for myosin.
Actin
Put these in the correct order:
A. Ca²⁺ binds to troponin
B. Myosin binds to actin
C. Ca²⁺ is released from the sarcoplasmic reticulum
D. Tropomyosin moves away from the binding site
C → A → D → B
Jake's motor neuron sends a perfectly normal signal to his skeletal muscle. His muscle fiber even receives the action potential.
BUT... his sarcoplasmic reticulum refuses to release Ca²⁺ because, apparently, it has decided to take the day off.
Jake asks: "So... am I still going to be able to contract my muscle?"
What do you tell him? Explain why.
No. Without Ca²⁺ being released, Ca²⁺ cannot bind to troponin, so tropomyosin remains blocking the myosin-binding sites on actin. Cross-bridge formation cannot occur, so the muscle cannot contract.
Your patient has normal motor neuron signaling and a normal muscle action potential. However, the sarcoplasmic reticulum isn't releasing Ca²⁺.
Where is the problem, and what happens to contraction?
The problem is Ca²⁺ release from the sarcoplasmic reticulum. Without Ca²⁺, troponin cannot initiate movement of tropomyosin, so myosin cannot bind effectively to actin and contraction cannot occur.
This ion is released from the sarcoplasmic reticulum and allows skeletal muscle contraction to begin.
Ca2+ (calcium)
Myosin has just attached to actin. What happens next?
The power stroke occurs, pulling the thin filament toward the center of the sarcomere (does anyone know what the purpose of ATP in this process is?)
Sarah comes into the ER complaining that her muscles aren't contracting properly.
The doctor runs some tests and discovers:
- Ca²⁺ is being released normally.
- ATP is available.
- Myosin cannot bind to actin.
What part of the contraction process should the doctor investigate, and why?
Troponin/tropomyosin regulation. If Ca²⁺ is present but myosin still cannot bind to actin, something is preventing the myosin-binding sites from becoming exposed
Your patient has plenty of Ca²⁺ and ATP, but myosin cannot bind to actin.
What part of the contraction process should you investigate?
Troponin/tropomyosin regulation of the myosin-binding sites on actin (does anyone know why?)
This protein normally blocks myosin-binding sites on actin when a muscle is relaxed.
Tropomyosin
A muscle fiber has received an action potential, but Ca²⁺ does not bind to troponin. What happens to the contraction process, and why?
Tropomyosin remains blocking the myosin-binding sites on actin, so cross-bridge formation cannot occur and contraction does not proceed.
Marcus comes to the ER after a very intense workout.
His muscles have:
- Ca²⁺
- Functional troponin
- Functional tropomyosin
- Myosin successfully attached to actin
BUT: his muscles suddenly can't continue the cross-bridge cycle because ATP is unavailable.
Marcus asks:
"If myosin is already attached to actin, why can't it just let go?"
How would you explain it to him? BONUS 100 points: What natural phenomenon occurs due to this?
ATP is required for myosin to detach from actin. Without ATP, the myosin head remains attached, preventing normal cross-bridge cycling. BONUS: rigor mortis!
Your patient can receive a motor neuron signal and release Ca²⁺ normally. Troponin and tropomyosin function normally. Myosin can bind to actin, but the muscle cannot continue cycling its cross-bridges.
What molecule is most likely missing, and why?
ATP