Model. (A) Diagram showing proposed complex assembled on the outer centriole for transport. Kinesin-1 interacts with the central region of PLP (aa584-1811). A yet-to-be-identified activator relieves autoinhibition of the Kinesin heavy chain, thereby enhancing MT landing rate as well as PLP interaction. (B) Diagram illustrating the centriole cycle of asymmetrically dividing neuroblasts (Fig. 8 A). (C i–vi) Diagram showing the consequence of defective centriole motility on the centriole cycle. (i) In early interphase, the centrioles disengage but remain at the apical side of the cell (Fig. 8, C–E). (ii) In mid interphase, both centrioles remain at the apical side of the cell, and the mother centriole (normally inactive) recruits PCM (Fig. 8 J and Fig. 9 A). (iii) The consequence of this is that at prophase, both centrosomes are activated at the apical side of the cell. They attempt to separate via the prophase centrosome separation pathway (Fig. 8, C–E). (iv) In some cells, the prophase centrosome separation and spindle alignment machinery is able to rescue the defective motility, resulting in a normal division with the neuroblast retaining the daughter centrosome. (v) In ∼30% of cells, the prophase centrosome separation pathway is able to rescue the centrosome separation; however, the NB will retain the mother centrosome (Fig. 9, E and F). (vi) In plp⁻ neuroblast, some cells fail to separate the two centrosomes by the prophase centrosome separation pathway. In this case, both centrosomes cluster at one spindle pole (Fig. 8 I); this will result in supernumerary centrioles in the next cell cycle (Fig. 8 H).