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. 2009 Aug 28;4(8):e6831. doi: 10.1371/journal.pone.0006831

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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A) Two modes of Aurora B mislocalization between condensin-depleted sister centromeres. Left panels: Localization of Aurora B kinase (anti-Aurora B antibodies) is shown relative to kinetochores (CREST sera) in control cells (mis RNAi), condensins-depleted cells (SMC2 RNAi) and in condensin-depleted cells treated by nocodazole (NZ). Significant separation between CREST and the bulk of Aurora B signals is evident in SMC2 RNAi cells. Inserts show magnified images representing individual sister kinetochore pairs from single optical sections. The arrows point to the Aurora B – free centromeres, which made a long excursion away from metaphase plate; asterisks indicate abnormally asymmetrical localization of Aurora B between condensin-depleted sister centromeres. Right panel: an example of preferentially reduced Aurora B staining at the stretched (highly merotelic) centromeres (indicated by brackets) within a sister pair. B) Monastrol arrest produces syntelic chromosomes in SMC2-depleted cells. Monastrol-treated cells, SMC2-depleted or control, were also treated with cold to stabilize microtubules. C) SMC2 depletion and Aurora B inactivation have similarly uncorrected merotelic metaphases. Analysis of cells released from monastrol arrest in the presence of condensins depletion, Aurora B inactivation (by ZM447439) or both showed that more than 90% of metaphases remain uncorrected after release (disorganized with high proportion of misattached microtubules), versus only 10% in control cells. Staining for HEC1 and Aurora B is shown for 20 min after release, HEC1 and microtubules – 40 min. D) SMC2 depletion and Aurora B inactivation have similar levels of abnormally attached kinetochores. Around 200 kinetochores (in cells stained for HEC1 and α-tubulin) were counted for each experiment 40 min after release from monastrol. Examples of qualifying images are shown for each category, determined on the basis of kinetochore position, stretching, and microtubule configurations. Statistical analysis confirmed that distribution of attachment types is indistinguishable between the condensins depletion, Aurora B inhibition and double treatment (Chi-square test: amphitelic 0.54 p>0.75, syntelic 0.35 p>0.85, merotelic 0.21 p>0.9).