Department of Molecular and Cellular Biology, University of California, Davis, Davis, CA 95616, USA.
J Cell Biol. 2011 Apr 18;193(2):285-94. doi: 10.1083/jcb.201011002. Epub 2011 Apr 11.
During mitosis, chromosome passenger complexes (CPCs) exhibit a well-conserved association with the anaphase spindle and have been implicated in spindle stability. However, their precise effect on the spindle is not clear. In this paper, we show, in budding yeast, that a CPC consisting of CBF3, Bir1, and Sli15, but not Ipl1, is required for normal spindle elongation. CPC mutants slow spindle elongation through the action of the bipolar kinesins Cin8 and Kip1. The same CPC mutants that slow spindle elongation also result in the enrichment of Cin8 and Kip1 at the spindle midzone. Together, these findings argue that CPCs function to organize the spindle midzone and potentially switch motors between force generators and molecular brakes. We also find that slowing spindle elongation delays the mitotic exit network (MEN)-dependent release of Cdc14, thus delaying spindle breakdown until a minimal spindle size is reached. We propose that these CPC- and MEN-dependent mechanisms are important for coordinating chromosome segregation with spindle breakdown and mitotic exit.
在有丝分裂过程中，染色体乘客复合物（CPCs）与后期纺锤体表现出良好的保守关联，并被认为与纺锤体稳定性有关。然而，它们对纺锤体的确切影响尚不清楚。在本文中，我们在芽殖酵母中表明，由 CBF3、Bir1 和 Sli15 组成的 CPC，但不包括 Ipl1，是正常纺锤体伸长所必需的。CPC 突变体通过双极动力蛋白 Cin8 和 Kip1 的作用减缓纺锤体伸长。同样减缓纺锤体伸长的 CPC 突变体也导致 Cin8 和 Kip1 在纺锤体中部区域的富集。综上所述，这些发现表明 CPCs 能够组织纺锤体中部区域，并有可能在力发生器和分子制动器之间切换马达。我们还发现，减缓纺锤体伸长会延迟 MEN（有丝分裂退出网络）依赖性的 Cdc14 释放，从而延迟纺锤体解体，直到达到最小纺锤体大小。我们提出，这些依赖 CPC 和 MEN 的机制对于协调染色体分离与纺锤体解体和有丝分裂退出非常重要。
