Any which way but loose
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《细胞学杂志》
Tanaka/Macmillan
A back-to-back arrangement of kinetochores is not needed for correct alignment on the mitotic spindle, as shown by Hilary Dewar, Tomoyuki Tanaka (University of Dundee, UK), and colleagues.
Sister chromatids are glued together by cohesin such that their kinetochores face opposing poles. This arrangement might thus prevent both chromatids from attaching to spindle microtubules from the same pole. But Tanaka's group shows that even when geometry fails, a tension-sensitive mechanism fixes any mistakes.
The authors messed with the usual geometry in two ways. First, they confronted yeast cells with a nonreplicating dicentric minichromosome. Its two kinetochores are not held in any fixed relative orientation, yet were efficiently attached to opposing poles. Second, normal chromosomes in cohesin mutants (which have attachment defects), were roughly linked by inhibiting topoisomerase II. This restored bipolar attachments. Thus, any connection that can produce tension is enough to ensure biorientation.
The tension-sensitive correction depends on the Ipl1 kinase, whose mammalian homologue, Aurora B, prevents monopolar attachments. This suggests that Ipl1 activity knocks off attachments until tension somehow stops it—perhaps by turning off the kinase, turning on a counteracting phosphatase, or pulling substrates away from the kinase.
Reference:
Dewar, H., et al. 2004. Nature. 10.1038/nature02328.(Dicentric chromosomes (green) reveal tha)
A back-to-back arrangement of kinetochores is not needed for correct alignment on the mitotic spindle, as shown by Hilary Dewar, Tomoyuki Tanaka (University of Dundee, UK), and colleagues.
Sister chromatids are glued together by cohesin such that their kinetochores face opposing poles. This arrangement might thus prevent both chromatids from attaching to spindle microtubules from the same pole. But Tanaka's group shows that even when geometry fails, a tension-sensitive mechanism fixes any mistakes.
The authors messed with the usual geometry in two ways. First, they confronted yeast cells with a nonreplicating dicentric minichromosome. Its two kinetochores are not held in any fixed relative orientation, yet were efficiently attached to opposing poles. Second, normal chromosomes in cohesin mutants (which have attachment defects), were roughly linked by inhibiting topoisomerase II. This restored bipolar attachments. Thus, any connection that can produce tension is enough to ensure biorientation.
The tension-sensitive correction depends on the Ipl1 kinase, whose mammalian homologue, Aurora B, prevents monopolar attachments. This suggests that Ipl1 activity knocks off attachments until tension somehow stops it—perhaps by turning off the kinase, turning on a counteracting phosphatase, or pulling substrates away from the kinase.
Reference:
Dewar, H., et al. 2004. Nature. 10.1038/nature02328.(Dicentric chromosomes (green) reveal tha)