Aurora B kinase, an immobile passenger!

The chromosomal passenger complex (CPC) is a key mitotic regulator composed of Aurora B kinase, Survivin, Borealin and INCENP.[1]The centromeric complex is involved in the correction of mis-attached microtubules by sensing tension on kinetochores. Aurora kinase phosphorylates microtubule binding factors, decreases their affinity for microtubules, and in turn, spindle microtubules are destabilized around kinetochores. The main Aurora B substrates involved in this dynamic are Ndc80/Hec1, a subunit of the Kinetochore-Microtubule-Network (KMN), and the microtubule-destabilizing factors MCAK and Stathmin/OP18. In the past, the main question was to elucidate the mechanism by which tension is sensed on centromere/kinetochore and how it may regulate Aurora B kinase activity.[2]Recently, Liu et al. have elegantly solved this question.[3]By using FRET-based bio-sensors and playing with the targeting of Aurora B, these authors have established that the spatial separation of Aurora B kinase from kinetochore substrates senses chromosome biorientation. In the absence of tension, kinetochore substrates in the vicinity of the kinase are phosphorylated and their affinity for microtubules is lowered. Kinetochore-microtubules attachments are thus destabilized. Conversely when tension is exerted, kinetochore substrates are pulled away from the kinase, their phosphorylation decreases and therefore microtubules are stabilized around kinetochores (Figure 1 A).[3, 4] Figure 1 Aurora B kinase, an immobile centromeric passenger