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. Author manuscript; available in PMC: 2014 Aug 26.
Published in final edited form as: Dev Cell. 2013 Aug 26;26(4):369–380. doi: 10.1016/j.devcel.2013.07.021

Figure 7. Model for coordinated control of Dynein and Khc7 during Pins-mediated spindle positioning.

Figure 7

(A) Cortical Pins recruits an “idling” Dynein through its TPR domain; the PinsTPR pathway alone is insufficient for any activity.

(B) Khc73 walks to MT plus ends where its N-terminus provides a physical link between MTs and cortical Pins; the Pinslinker pathway is sufficient for partial spindle orientation activity through cortical-microtubule capture.

(C) Khc73 transports NudE to MT plus ends, bringing NudE within proximity to activate cortical Dynein. Activated Dynein moves toward MT minus ends to generate the necessary cortical pulling required for robust spindle positioning; the PinsTPR+linker pathway is sufficient for full spindle orientation. NudE was depicted to associate with the ATPase region of cytoplasmic Dynein for clarity.

(D) Schematic representation of the genes and the functions of PinsTPR (black) and Pinslinker (green) pathway components for Pins-mediated spindle positioning. The PinsTPR pathway components 14-3-3 ε, 14-3-3 ζ, and NudE have roles outside of PinsTPR pathway function (gray) that may be essential for proper Pins-mediated spindle positioning.