Models of the regulation of dynein activity via the CP–RS mechanosignaling. (A and B, top) Schematic diagrams of C. reinhardtii cells and flagella showing the orientation of cross sections of axonemes relative to the cell and bending direction. The 9 + 2 structures are viewed from the base. DMT numbering was adapted from Hoops and Witman (1983). (A, bottom) In a straight flagellum, CP projections are not in contact with RS heads, and all dyneins are in the resting state. (B, bottom) When a flagellum makes a principal bend (red arrows), the circular arrangement of the nine DMTs is distorted (Lindemann and Mitchell, 2007), and C1 is located on the outer side (closest to DMT 1) of the curved flagellum (Mitchell, 2003). As a result of this distortion, C1a projections collide with RS heads and modulate the dynein activity on DMT 3 (or DMTs 2–4). (C) When streptavidin molecules bind to RS heads, nonphysiological CP–RS contacts occur on many DMTs, and irregular activation or inactivation of ODA causes flagellar paralysis. (D) In a cpc1 flagellum, the absence of C1b projections does not cause a serious motility defect (Mitchell and Sale, 1999). The remaining C1a projection alone can modulate dynein activity through a collision with RS heads at bent regions of the flagellum. (E) The absence of C1a projections in pf6 severely impairs motility (Dutcher et al., 1984; Rupp et al., 2001). Loss of the CP–RS contact by C1a projection would result in failure of dynein regulation. (F) Addition of tags to RS heads restores CP–RS contacts in bent regions of the flagellum, and dyneins (mainly ODAs) are modulated through collisions between a remnant of the C1a projection or other CP projections and the tagged RS heads. WT, wild type.