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Figure 4


Fig. 4. A model for how Aurora-A controls centrosomal MT stability. TACC protein is exclusively phosphorylated by Aurora-A (Aur) at the centrosome (in yellow). The targeting of TACC to the centrosome may be achieved in two ways: direct phosphorylation by Aurora-A or by Aurora-A-phosphorylated NDEL1. TACC can only bind MTs (in green) when complexed with the MT-stabilising protein ch-TOG/XMAP215 (TOG), and together they are required to counter the MT-destabilising activity of MCAK/XKCM1 (MCAK). Aurora-A-mediated phosphorylation of TACC promotes the binding of TACC-TOG to MT minus-ends, where they protect MTs from MCAK-induced destabilisation. Once bound to MT ends, TACC becomes dephosphorylated. The TACC-TOG complex could have additional roles on the plus-ends of MTs. It therefore stabilises centrosome-associated MTs in two ways: by protecting their minus ends from MCAK activity and by stabilising MTs as they polymerise. When endogenous TACC is replaced with non-phosphorylatable TACC, centrosomal TACC levels may be reduced. Furthermore, TACC-TOG fails to accumulate on MT minus-ends and centrosomal MTs are no longer shielded from MCAK activity.





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