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. 2009 Nov 30;187(5):597–605. doi: 10.1083/jcb.200905026

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© 2009 Rahmani et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jcb.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 2. — bubR1-KD mutants are checkpoint competent, but bubR1-KEN mutants are checkpoint defective. (A–C) Representative fields of cells from larval brains incubated in colchicine for 60 min. WT (A) or bubR1-KD mutant (B) cells accumulate in prometaphase, whereas bubR1-KEN mutants do not (C). However, PSCS is common in both mutants (boxed areas and insets in B and C). (D and E) The very high mitotic density caused by mutations in asp (D) is suppressed in bubR1-KEN asp double mutants (E). The number of anaphases (very rare in asp) also rises (oval in E). See Table I. Yellow circles and ovals mark mitotic cells in the fields. Orcein-stained preparations are shown. Bar, 10 µm.