Tension Sensing by Aurora B Kinase is Independent of Survivin-Based Centromere Localization

Accurate segregation of the replicated genome requires chromosome biorientation on the spindle. Biorientation is ensured by Aurora B kinase, a member of the 4-subunit chromosomal passenger complex (CPC)(1,2). Localization of the CPC to the inner centromere is central to the current model for how tension ensures chromosome biorientation—kinetochore-spindle attachments 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(3–5). Here we show that an engineered truncation of the INCENP/Sli15 subunit of budding yeast CPC that eliminates association with the inner centromere nevertheless supports proper chromosome segregation during both mitosis and meiosis. Truncated INCENP/Sli15 suppresses the deletion phenotypes of the inner centromere-targeting proteins Survivin/Bir1, Borealin/Nbl1, Bub1 and Sgo1(6). Unlike wildtype INCENP/Sli15, truncated INCENP/Sli15 localizes to pre-anaphase spindle microtubules. Premature targeting of full-length INCENP/Sli15 to microtubules by preventing Cdk1 phosphorylation also suppresses inviability of Survivin/Bir1 deletion. These results suggest that activation of Aurora B/Ipl1 by clustering either on chromatin or on microtubules is sufficient for chromosome biorientation.