The chromosomal passenger complex (CPC), consisting of INCENP, survivin, borealin and the kinase Aurora B, has multiple roles in mitosis. It is believed that the localization of Aurora B to the inner centromere is essential for its role in correcting erroneous kinetochore–microtubule attachments. However, Campbell and Desai have discovered that in budding yeast, accurate chromosome biorientation occurs in the absence of centromere-localized CPC (Nature 497, 118–121; 2013).

The authors found that an INCENP (Sli15) mutant with a truncated N-terminus (Sli15(ΔNT)) that is unable to bind survivin, known to target the CPC to centromeres, did not affect viability. The Sli15(ΔNT) cells failed to show defects in several assays for chromosome segregation and biorientation despite the lack of Sli15(ΔNT) and Aurora B (Ipl1) between sister kinetochore clusters (the localization corresponding to the inner centromere in other species). However, the Sli15(ΔNT)–Ipl1 complex accumulated prematurely at spindle microtubules. As microtubules can activate Aurora B, the authors suggest that this premature clustering on microtubules is sufficient for its role in biorientation, an idea they confirm by prematurely localizing Sli15 on microtubules by other means. This could also explain how truncated Sli15 can suppress the phenotypes of mutations in genes whose products are known to target the CPC to centromeres.

These data, together with previous findings by the Earnshaw group (J. Cell Biol. 183, 279–296; 2008) demonstrating viability of chicken DT40 cells in the absence of centromere-localized CPC, may call for a revised view on how Aurora B exerts its role in promoting proper attachment.