Human Physiology ❮ 189
energy, and causing it to elegantly tilt its head to one side... sliding the beautiful actin
toward the center of the sarcomere (Figure 15.6b). The two part ways when myosin again
binds to ATP, bringing us back to where we started (Figure 15.6a).
:::Applause:::
Control mechanisms are often mentioned on the AP Biology exam and make good essay
material. It would be really annoying and awkward if our muscles were contracting all the
time. So, it makes sense that there must be some way to control the contraction. Myosin is
only able to dance with actin if a regulatory protein, known as tropomyosin,is not blocking
the attachment site on actin. The key to the removal of tropomyosin is the presence of cal-
cium ions. Tropomyosin is also bound to anotherregulatory protein known as troponin.
Calcium causes these two to do their own little dance and shuffle away from the actin-myosin
binding site. This allows the actin-myosin dance to occur and muscle contraction to follow.
When the calcium is gone, the dance is complete, and the filaments separate from each other.
What causes this calcium release seen in muscle contraction? This brings us back to the
neuromuscular junction mentioned not too long ago. Nervous impulses from motor neu-
rons cause the release of acetylcholine into the neuromuscular junction. Acetylcholine
binds to the muscle cell and initiates a series of reactions that culminates in the dumping
of calcium from its storage facility—the sarcoplasmic reticulum. This calcium finds tro-
ponin, binds to it, and lets the dance begin.
= Thin filament (actin)
= Thick filament (myosin)
(a)
(b)
Figure 15.6 Actin-myosin interaction: (a) relaxed muscle; (b) contracted muscle.
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