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Drosophila Ensconsin/MAP7 controls spindle length, centrosome separation in brain Neuroblasts (NBs) and asymmetric transport in oocytes. The control of spindle length by Ensconsin is Kinesin-1 independent but centrosome separation and oocyte transport requires targeting of Kinesin-1 to microtubules by Ensconsin. However, the molecular mechanism used for this targeting remains unclear. Ensconsin/MAP7 contains a microtubule-binding domain (MBD) and a Kinesin-binding domain (KBD). Rescue experiments show that only full length Ensconsin restores the spindle length phenotype. KBD expression rescues ensc centrosome separation defects in NBs, but not the fast oocyte streaming and the localization of Staufen and Gurken. Interestingly, the KBD can stimulate Kinesin-1 targeting to MTs in vivo and in vitro. We propose that the KBD/Kinesin-1 is a minimal activation module that increases Kinesin-1 affinity for MTs. Addition of the MBD present in full length Ensconsin allows this process to occur directly on the microtubule and triggers higher Kinesin-1 targeting. This dual regulation by Ensconsin is essential for optimal Kinesin-1 in oocytes, but not in NBs, illustrating the importance of adapting Kinesin-1 recruitment to different biological contexts.

Dual control of Kinesin-1 recruitment to microtubules by Ensconsin inDrosophilaneuroblasts and oocytes