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有读书笔记有附件Protein Phosphatase 1 Regulates Exit from the Spindle Checkpoint in Budding Yeast

热1 阿平 添加于 2009-9-2 03:35 | 4222 次阅读 | 0 个评论

  •  作 者

    Pinsky BA, Nelson CR, Biggins S

  •  摘 要

    Accurate chromosome segregation depends on sister kinetochores coming under tension when they make bioriented attachments to microtubules from opposite poles. The spindle checkpoint halts the cell cycle in response to defects in generating proper attachments or tension on kinetochores , although the precise signal that triggers the checkpoint is unclear because tension and attachment are coupled . The target of the checkpoint is the Cdc20 protein, which initiates the anaphase-promoting complex (APC)-dependent degradation of the anaphase inhibitor Pds1/securin . Although the molecular details of spindle checkpoint activation are still being elucidated, phosphorylation by at least four kinases is a crucial requirement . However, less is known about the mechanisms that silence the checkpoint after kinetochores biorient. Here, we show that the catalytic subunit of the budding yeast protein phosphatase 1 (PP1) homolog, Glc7, regulates exit from the checkpoint. Glc7 overexpression prevents spindle checkpoint activation in response to both tension and attachment defects. Although glc7 mutant cells are able to efficiently release from a non-checkpoint-mediated metaphase arrest, they are uniquely sensitive to transient spindle checkpoint activation as a result of a failure in spindle checkpoint exit. We therefore propose that PP1 activity silences the checkpoint by reversing key phosphorylation events.

  •  详细资料

    • 文献种类: Journal Article
    • 期刊名称: Current Biology : CB
    • 期刊缩写: Curr Biol
    • 期卷页: 2009年
    • 地址: Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, PO Box 19024, Seattle, WA 98109, USA
    • ISBN: 1879-0445
    • 备注:PMID:19592248

  • 学科领域 生物医药 » 生物学

  •  标 签

    PP1  有丝分裂  磷酸化  protein phoshatase 1 

  • 相关链接 DOI URL 

  •  阿平 的文献笔记  订阅

    PP1是budding yeast克服spindle checkpoint的关键蛋白

     

     

    这篇文章用budding yeast中高表达或者突变glc7（PP1）作为模型，使用了两大工具，一是securin，二是MPS1诱导的checkpoint arrest。

    高表达PP1可导致染色体异常分裂，并且可导致securin的提早降解，突变glc7则会让securin无法降解。这样正反两方面来证明，基本上翻来覆去讲，有点让人烦了为止。

    但是最后一个方法值得肯定，那就是如何确定glc7带来的改变一定是在克服spindle checkpoint这个环节，而不是其后的cdc20的问题而导致的APC/C失活。方法就是把删除了内源cdc20，但有转入了pMET-CDC20控制表达的细胞用methionine停滞到metaphase，然后洗去methionine，这样cdc20才能得以表达，以这个时间框作为研究对象，发现该时间框内，glc7是否突变没有影响，从而来印证glc7是在之前的一个环节就发挥作用了的，那就是checkpoint阶段。此结论和我此前看到另一篇在mammalian cell中的结论有冲突（mitosis persists with cdk activity absence）

    同期杂志中还有一篇双飞文章，看看这篇

    http://www.xinkexue.com/bib-ref-refid-791.html

    仔细再看了图片结合

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