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The mitotic checkpoint complex binds a second CDC20 to inhibit active APC/C

机译：有丝分裂检查点复合物结合第二个CDC20抑制活性APC / C

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"纺锤体组装检查点"通过延迟染色体分离、直到它们都通过其动粒正确附着到微管上来防止过早的细胞分裂。这种"等待"信号来自未附着的动粒，涉及"后期促进复合物"APC/C辅助活化剂CDC20通过有丝分裂检查点复合物MCC发生的失活。现在，Daisuke Izawa &Jonathon Pines发现，MCC能结合和抑制两个CDC20分子——一个被隔离在MCC内，另一个已经结合和激发了APC/C。这便提出了一个模型，在其中MCC本身也许就是抑制胞质APC/C的一个可扩散的"等待"信号。%The spindle assembly checkpoint (SAC) maintains genomic stability by delaying chromosome segregation until the last chromosome has attached to the mitotic spindle. The SAC prevents the anaphase promoting complex/cyclosome (APC/C) ubiquitin ligase from recognizing cyclin B and securin by catalysing the incorporation of the APC/ C co-activator, CDC20, into a complex called the mitotic checkpoint complex (MCC). The SAC works through unattached kinetochores generating a diffusible 'wait anaphase' signal that inhibits the APC/C in the cytoplasm, but the nature of this signal remains a key unsolved problem. Moreover, the SAC and the APC/C are highly responsive to each other: the APC/C quickly targets cyclin B and securin once all the chromosomes attach in metaphase, but is rapidly inhibited should kinetochore attachment be perturbed. How this is achieved is also unknown. Here, we show that the MCC can inhibit a second CDC20 that has already bound and activated the APC/C. We show how the MCC inhibits active APC/C and that this is essential for the SAC. Moreover, this mechanism can prevent anaphase in the absence of kinetochore signalling. Thus, we propose that the diffusible 'wait anaphase' signal could be the MCC itself, and explain how reactivating the SAC can rapidly inhibit active APC/C.
机译："纺锤体组装检查点"通过延迟染色体分离、直到它们都通过其动粒正确附着到微管上来防止过早的细胞分裂。这种"等待"信号来自未附着的动粒，涉及"后期促进复合物"APC/C辅助活化剂CDC20通过有丝分裂检查点复合物MCC发生的失活。现在，Daisuke Izawa &Jonathon Pines发现，MCC能结合和抑制两个CDC20分子——一个被隔离在MCC内，另一个已经结合和激发了APC/C。这便提出了一个模型，在其中MCC本身也许就是抑制胞质APC/C的一个可扩散的"等待"信号。%The spindle assembly checkpoint (SAC) maintains genomic stability by delaying chromosome segregation until the last chromosome has attached to the mitotic spindle. The SAC prevents the anaphase promoting complex/cyclosome (APC/C) ubiquitin ligase from recognizing cyclin B and securin by catalysing the incorporation of the APC/ C co-activator, CDC20, into a complex called the mitotic checkpoint complex (MCC). The SAC works through unattached kinetochores generating a diffusible 'wait anaphase' signal that inhibits the APC/C in the cytoplasm, but the nature of this signal remains a key unsolved problem. Moreover, the SAC and the APC/C are highly responsive to each other: the APC/C quickly targets cyclin B and securin once all the chromosomes attach in metaphase, but is rapidly inhibited should kinetochore attachment be perturbed. How this is achieved is also unknown. Here, we show that the MCC can inhibit a second CDC20 that has already bound and activated the APC/C. We show how the MCC inhibits active APC/C and that this is essential for the SAC. Moreover, this mechanism can prevent anaphase in the absence of kinetochore signalling. Thus, we propose that the diffusible 'wait anaphase' signal could be the MCC itself, and explain how reactivating the SAC can rapidly inhibit active APC/C.

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  • 来源
    《Nature》 |2015年第7536期|631-634a2-a3|共6页
  • 作者

    Daisuke Izawa; Jonathon Pines;

  • 作者单位

    The Gurdon Institute and Department of Zoology, Tennis Court Road, Cambridge CB2 1QN, UK;

    The Gurdon Institute and Department of Zoology, Tennis Court Road, Cambridge CB2 1QN, UK;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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