Before we move on to seeing these proteins in action we must discuss the very important aspect of muscle contraction… being able to turn it on and off. Take a deep breath in, now blow it out. You are able to do that because you turned on the contraction of your diaphragm to take the breath in, and then turned it off to blow the air out by relaxing the diaphragm muscle. If you are unable to turn contraction on and off, muscles may contract and stay that way until they eventually fatigue.You can see the negative implications of that with the deep breath we just took.
So how do we turn contraction on and off? We use regulatory proteins troponin and tropomyosin, both of which are located on the actin (thin) filament. Tropomyosin is a rope like structure that overlay the myosin binding sites on the actin subunits. By blocking the binding sites myosin cannot bind to actin even though they are in close proximity to one another, and the sarcomere will not begin sliding to shorten. I think of it as a door that is closed between actin and myosin. They cannot bind and perform contraction if the closed door (tropomyosin) is in place. The other regulatory protein is troponin, which is composed of 3 subunits. One of the subunits binds to tropomyosin to connect the 2 regulatory proteins together, and another of the subunits binds to calcium. When the muscle is stimulated to contract, calcium is released from its storage facility - the sarcoplasmic reticulum - into the sarcoplasm of the cell. As the calcium travels through the cell it will encounter and bind to troponin. I think of calcium as the key (just the right key, or ion, to unlock the door – not Na or K, etc.) and troponin as the lock on the door, since the two regulatory proteins are attached. When the calcium ion "key" binds with troponin "the lock," it changes the shape of the troponin protein and causes it to rotate, just like turning a key in a lock. As it rotates it pulls tropomyosin off of the binding sites or "opens the door"– remember the 2 regulatory proteins are attached so when one moves so does the other. With tropomyosin out of the way the myosin can reach the actin and start the process of contraction.
Simply put, here is a summary of how to turn contraction on:
1. Calcium is released from the sarcoplasmic reticulum
2. Calcium binds to troponin
3. Troponin moves and pulls tropomyosin off of the myosin binding sites "moving the door"
4. With the binding sites now available the steps of the Sliding Filament Theory begin and contraction occurs.
Now that we can clearly see calcium is the signal to turn contraction on we can extrapolate that when calcium leaves the contraction is turned off. This happens by simply having the opposite of the steps listed above.
To turn contraction off:
1. Calcium is actively pumped back into the sarcoplasmic reticulum and "returns to storage" (requiring the presence of ATP, right?)
2. Calcium (key) is no longer binding with troponin (the lock)
3. Troponin moves and tropomyosin rolls back onto the myosin binding sites "closing the door"
4. With the binding sites no longer available (the door is closed over the opening again) the steps of the Sliding Filament Theory end and contraction ceases.
Understanding this process while making part of contraction clearer still leaves us with many questions. How does the calcium get released? What is the signal for this to occur? Where does this signal come from? We will address these questions in our next segment about the neuromuscular junction.
Video 3. Calcium Troponin Tropomyosin Interaction - "Key Lock Door" Analogy (opens YouTube in new window)
Video 4. Sliding Filament Model (opens Youtube in new window)
Activity not available on mobile devices (description)
