Abstract:35The strength of the Spindle Assembly Checkpoint (SAC) depends on the amount of the 36 Mad1-C-Mad2 heterotetramer at kinetochores but also on its binding to Megator/Tpr at 37 nuclear pore complexes (NPCs) during interphase. However, the molecular underpinnings 38 controlling the spatiotemporal redistribution of Mad1-C-Mad2 as cells progress into mitosis 39 remain elusive. Here, we show that Mps1-mediated phosphorylation of Megator/Tpr 40 abolishes its interaction with Mad1 in vitro and in Drosophila cells. Ti… Show more
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