FEEDBACK-CONTROL OF MITOSIS IN BUDDING YEAST
FEEDBACK-CONTROL OF MITOSIS IN BUDDING YEAST
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DOI：
10.1016/0092-8674(81)90015-5
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发表时间：
1991-08-09
期刊：
影响因子：
64.5
通讯作者：
MURRAY, AW
中科院分区：
文献类型：
--
作者：
LI, R;MURRAY, AW
我们研究了反馈控制，以防止未完全组装的纺锤体细胞离开有丝分裂。我们分离到对抗微管药物苯菌灵敏感的芽期酵母突变株。有丝分裂停滞缺陷(MAD)突变体是苯菌灵敏感突变体的一个亚类，在苯菌灵存在的情况下，有丝分裂的完成不会延迟，并且由于过早退出有丝分裂而死亡。MAD突变体的一些特性表明，它们在有丝分裂退出的反馈控制方面存在缺陷：它们被苯菌灵杀死需要通过有丝分裂；它们对苯菌灵的敏感性可以被一种独立的延迟有丝分裂退出的方法抑制；它们有正常的微管；它们染色体丢失的频率增加。我们克隆了MAD2，它编码一种假定的钙结合蛋白，其干扰是致命的。我们讨论了反馈控制在细胞周期中协调事件中的作用。
We have investigated the feedback control that prevents cells with incompletely assembled spindles from leaving mitosis. We isolated budding yeast mutants sensitive to the anti-microtubule drug benomyl. Mitotic arrest-deficient (mad) mutants are the subclass of benomyl-sensitive mutants in which the completion of mitosis is not delayed in the presence of benomyl and that die as a consequence of their premature exit from mitosis. A number of properties of the mad mutants indicate that they are defective in the feedback control over the exit from mitosis: their killing by benomyl requires passage through mitosis; their benomyl sensitivity can be suppressed by an independent method for delaying the exit from mitosis; they have normal microtubules; and they have increased frequencies of chromosome loss. We cloned MAD2, which encodes a putative calcium-binding protein whose disruption is lethal. We discuss the role of feedback controls in coordinating events in the cell cycle.