The movement of a cilium or a flagellum is produced by the bending of its core, which is called the axoneme. The axoneme is composed of microtubules and their associated proteins, arranged in a distinctive and regular pattern. Nine special doublet microtubules (comprising one complete and one partial micro-tubule fused together so that they share a common tubule wall) are arranged in a ring around a pair of single microtubules (Figure 16–63). Almost all forms of motile eukaryotic flagella and cilia (from protozoans to humans) have this characteristic arrangement. The microtubules extend continuously for the length of the axoneme, which can be 10–200 μm. At regular positions along the length of the microtubules, accessory proteins cross-link the microtubules together.
Figure 16–63 The arrangement of microtubules in a flagellum or cilium. (A) Electron micrograph of the flagellum of a green-alga cell (Chlamydomonas) shown in cross section, illustrating the distinctive “9 + 2” arrangement of microtubules. (B) Diagram of the parts of a flagellum or cilium. The various projections from the microtubules link the microtubules together and occur at regular intervals along the length of the axoneme.
(C) High-resolution electron tomography image of an outer doublet microtubule showing structural details and features inside the microtubules called microtubule inner proteins (MIPs). (A, courtesy of Lewis Tilney; C, courtesy of Daniela Nicastro.) 942 Chapter 16: The Cytoskeleton
Molecules of axonemal dynein form bridges between the neighboring doublet microtubules around the circumference of the axoneme (Figure 16–64). When the motor domain of this dynein is activated, the dynein molecules attached to one microtubule doublet (see Figure 16–59) attempt to walk along the adjacent microtubule doublet, tending to force the adjacent doublets to slide relative to one another, much as actin thin filaments slide during muscle contraction. However, the presence of other links between the microtubule doublets prevents this sliding, and the dynein force is instead converted into a bending motion (Figure 16–65).
In humans, hereditary defects in axonemal dynein cause a condition called primary ciliary dyskinesia or Kartagener’s syndrome. This syndrome is characterized by inversion of the normal asymmetry of internal organs (sinus inversus) due to disruption of fluid flow in the developing embryo, male sterility due to immotile sperm, and a high susceptibility to lung infections due to paralyzed cilia being unable to clear the respiratory tract of debris and bacteria.
Bacteria also swim using cell-surface structures called flagella, but these do not contain microtubules or dynein and do not wave or beat. Instead, bacterial flagella are long, rigid helical filaments, made up of repeating subunits of the protein flagellin. The flagella rotate like propellers, driven by a special rotary motor embedded in the bacterial cell wall. The use of the same name to denote these two very different types of swimming apparatus is an unfortunate historical accident.
Many cells possess a shorter, nonmotile counterpart of cilia and flagella called the primary cilium. Primary cilia can be viewed as specialized cellular compartments or organelles that perform a wide range of cellular functions, but share