Importance of flagellum motility revealed by procyclic motility mutants. Schematic representations of motility phenotypes in procyclic Trypanosoma brucei flagellum mutants. Wild-type (WT) cell movement is helical with the flagellum tip leading. RNA interference knockdown of flagellar protein expression leads to a variety of motility phenotypes. “Dizzy” mutants, such as trypanin knockdown mutants (Hutchings et al., 2002), retain a vigorously beating flagellum, but are unable to move directionally, and instead tumble in place. “Reverse” motility is observed when subunits of the outer dynein motors, such as DNAI1 (Branche et al., 2006) or LC1 (Baron et al., 2007a) are targeted. These mutants exhibit a reverse, base-to-tip beat and move backward with the flagellum tip trailing. “Paralyzed” mutants, such as central pair and radial spoke mutants (Branche et al., 2006; Ralston et al., 2006) are incapable of movement at the cellular level. Some paralyzed mutants have flagella that are able to beat, while other mutants have more severe defects and are only capable of erratic twitching motions. “Lethal” defects arise in mutants with severe flagellar paralysis (Baron et al., 2007b).