The Ca2+-dependence of vertebrate skeletal muscle contraction, and hence its dependence on commands transmitted via nerves, is due entirely to a set of specialized accessory proteins that are closely associated with the actin thin filaments. One of these accessory proteins is a muscle form of tropomyosin, the elongated protein that binds along the groove of the actin filament helix. The other is troponin, a complex of three polypeptides, troponins T, I, and C (named for their tropomyosin-binding, inhibitory, and Ca2+-binding activities, respectively). Troponin I binds to actin as well as to troponin T. In a resting muscle, the troponin I–T complex pulls the tropomyosin out of its normal binding groove into a position along the actin filament that interferes with the binding of myosin heads, thereby preventing any force-generating interaction. When the level of Ca2+ is raised, troponin C—which binds up to four molecules of Ca2+—causes troponin I to release its hold on actin. This allows the tropomyosin molecules to slip back into their normal position so that the myosin heads can walk along the actin filaments (Figure 16–36). Troponin C is closely related to the ubiquitous Ca2+-binding protein calmodulin (see Figure 15–33); it can be thought of as a specialized form of calmodulin that has acquired binding sites for troponin I and troponin T, thereby ensuring that the myofibril responds extremely rapidly to an increase in Ca2+ concentration.
In smooth muscle cells, so called because they lack the regular striations of skeletal muscle, contraction is also triggered by an influx of calcium ions, but the regulatory mechanism is different. Smooth muscle forms the contractile portion of the stomach, intestine, and uterus, as well as the walls of arteries and many other structures requiring slow and sustained contractions. Smooth muscle is 0.5 µm
Figure 16–35 T tubules and the sarcoplasmic reticulum. (A) Drawing of the two membrane systems that relay the signal to contract from the muscle cell plasma membrane to all of the myofibrils in the cell. (B) Electron micrograph showing a cross section of a T tubule. Note the position of the large Ca2+-release channels in the sarcoplasmic reticulum membrane that connect to the adjacent T-tubule membrane. (C) Schematic diagram showing how a Ca2+-release channel in the sarcoplasmic reticulum membrane is thought to be opened by the activation of a voltage-gated Ca2+ channel (Movie 16.5). (B, courtesy of Clara Franzini-Armstrong.)