Tension sensing by Aurora B kinase is independent of survivin-based centromere localization

摘要

Accurate segregation of the replicated genome requires chromosome biorientation on the spindle. Biorientation is ensured by Aurora B kinase (Ipll), a member of the four-subunit chromosomal passenger complex (CPC). Localization of the CPC to the inner centromere is central to the current model for how tension ensures chromosome biorientation: kinetochore-spindle attachments that are not under tension remain close to the inner centromere and are destabilized by Aurora B phosphorylation, whereas kinetochores under tension are pulled away from the influence of Aurora B, stabilizing their microtubule attachments. Here we show that an engineered truncation of the Slil5 (known as INCENP in humans) subunit of budding yeast CPC that eliminates association with the inner centromere nevertheless supports proper chromosome segregation during both mitosis and meiosis. Truncated SU15 suppresses the deletion phenotypes of the inner-centromere-targeting proteins survivin (Birl), borealin (Nbll), Bubl and Sgol (ref. 6). Unlike wild-type Slil5, truncated Slil5 localizes to pre-anaphase spindle microtubules. Premature targeting of full-length SH15 to microtubules by preventing Cdkl (also known as Cdc28) phosphorylation also suppresses the inviability of Birl deletion. These results suggest that activation of Aurora B kinase by clustering either on chromatin or on microtubules is sufficient for chromosome biorientation.