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有读书笔记有附件Centromeric Aurora-B activation requires TD-60, microtubules, and substrate priming phosphorylation

阿平 添加于 2009-5-23 07:34 | 3465 次阅读 | 0 个评论

  •  作 者

    Rosasco-Nitcher SE, Lan W, Khorasanizadeh S, Stukenberg PT

  •  摘 要

    The chromosome passenger complex (CPC) controls chromosome congression, kinetochore-microtubule attachments, and spindle checkpoint signaling during mitosis. Aurora-B kinase is the catalytic subunit of the CPC. To understand how a single kinase can regulate such diverse events, we have investigated the activation of Aurora-B and describe two distinct activation mechanisms. First, Aurora-B activation in vitro requires two cofactors, telophase disc-60kD (TD-60) and microtubules. TD-60 is critical to localize both the CPC and Haspin kinase activity to centromeres and thus regulates Aurora-B at several levels. Second, Aurora-B substrates can inhibit kinase activation, and this is relieved by phosphorylation of these substrates by the centromeric kinases Plk1 and Haspin. These regulatory mechanisms suggest models for phosphorylation by Aurora-B of centromeric substrates at unaligned chromosomes and merotelic attachments.

  •  详细资料

    • 关键词: Animals; Cell Cycle Proteins/metabolism; Centromere/*metabolism; Chromosomal Proteins, Non-Histone/*metabolism; Enzyme Activation; Histones/metabolism; Intracellular Signaling Peptides and Proteins/metabolism; Kinesin/metabolism; Microtubules/*metabolism; *Mitosis; Phosphorylation; Protein-Serine-Threonine Kinases/*metabolism; Xenopus/metabolism; Xenopus Proteins/*metabolism
    • 文献种类:期刊
    • 期刊名称: Science (New York, N.Y.)
    • 期刊缩写: Science
    • 期卷页: 2008年  第319卷 第5862期 469-472页
    • 地址: Department of Biochemistry and Molecular Genetics, University of Virginia Medical School, Charlottesville, VA 22908, USA
    • ISBN: 1095-9203
    • 备注:PMID:18218899

  •  标 签

    Haspin  组蛋白  Aurora 

  • 相关链接 DOI URL 

  •  附 件

    PDF附件全文  PDF附件附属材料 

  •  阿平 的文献笔记  订阅

    少量TD-60就可localize Aurora B到centromere，大量TD-60就可激活Aurora B，这点用H3-S10和H3-T3的磷酸化可以说明问题。
    microtubule也能激活Aurora B。还有就是其他kinase（如polo）先priming一下底物，然后由aurora B接受。而haspin对aurora B保持活性意义重大。

    比如加入未磷酸化的H3-S10底物到激酶活性检验体系中，发现aurora B的激酶活性减弱了很多（以AI为检测底物的情况下），但是当H3-T3被磷酸化后，这种抑制作用又被取消了。这个make sense得很！充分解释了为什么Aurora B在centromere里是可以被活化的。也间接说明Haspin可以活化Aurora B。
    还 有一点也很有趣，未磷酸化的H3可以紧紧bind CPC，而磷酸化的H3的这种bind就很弱，这就让我想到为什么最后CPC会离开chromosome的原因，那就是chromosome领酸化程度太 高了，CPC已经再也抓不住chromosome了，然后刚好被microtubule一拉，就拉倒central spindle上去了。

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