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. 2003 Aug 18;162(4):551–563. doi: 10.1083/jcb.200303167

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Copyright © 2003, The Rockefeller University Press

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Figure 4. — Microtubule depolymerization causes CENP-E ^Δ/Δ cells to arrest in mitosis with reduced amounts of BubR1, Mad1, and Mad2 on their kinetochores. (A) FACS^® profile of propidium iodide–stained CENP-E^+/+ cells (left column) and CENP-E^Δ/Δ cells (right column) after microtubule depolymerization with colcemid or microtubule stabilization with taxol. 75% of these primary cells are cycling. (B) Immunofluorescence of CENP-E^+/+ cells (left column) and CENP-E^Δ/Δ cells (right column) after a 30-min treatment with 200 ng/ml colcemid, showing that CENP-E is required for maximal kinetochore targeting of BubR1, Mad1, and Mad2 (green). DNA is shown in blue. Bar, 2.5 μm. (C) Quantitation of the normalized integrated intensities of the kinetochore signals in B. ≥800 kinetochores from ≥10 cells were quantitated for each bar. Error bars represent standard errors. **, P < 0.001.