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. 2019 Jul 15;18(17):2006–2025. doi: 10.1080/15384101.2019.1634954

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© 2019 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

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Figure 5. — Plk1 docking on INCENPa is a prerequisite for centromeric enrichment of CPCa during late prophase. (a) Plk1 localized on centrosomes and briefly enriched on centromeres during late prophase concomitant with the onset of centromeric H3pS28. (b) Plk1 colocalized with Aurora B on centromeres during late prophase and on the central spindle during anaphase. Inhibition of Plk1 (BI2536) abolished Plk1 staining on centromeres and centrosomes, and Aurora B spread along chromosome arms. (c) Plk1 inhibition resulted in centromeric H3pS28 and INCENPa spreading throughout chromosomes, without affecting CenH3 on centromeres. The INCENPa^S209A mutant failed to localize to centromeres. The graph on the right shows the percentage of pro-metaphase cells that showed nuclear or centromeric INCENP localization for INCENPa WT or the S₂₀₉A mutant. Mean values (n = 3) are shown with SE. Bars, 3 µm.