mik1和wee1在抑制cdc2的氨酸酸化中进行合作
K Lundgren1, N Walworth, R Booher
1Howard Hughes Medical Institute, Cold Spring Harbor Laboratory, New York 11724.
Cell
|March 22, 1991
概括
在S. pombe中,mik1和wee1基因酶通过控制cdc2酸化来调节细胞分裂. 这两种激酶的损失导致致命的细胞周期绕道,这表明它们对于M阶段检查点至关重要.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 遗传学 是一个遗传学.
背景情况:
- 微1激酶在调节cdc2活性时对抗Cdc25酸酶.
- 韦1在cdc2的氨酸酸化中的确切作用尚不清楚.
- Mik1是一种与Wee1相关的酶,其功能不明.
研究的目的:
- 研究Mik1在S. pombe细胞周期调节中的作用.
- 为了确定Mik1和Wee1.1之间的功能关系.
- 阐明M阶段cdc2调节的机制.
主要方法:
- 在S. pombe中构建和分析mik1和wee1无基因突变.
- 评估M阶段检查点和细胞周期进展.
- 在各种突变基因背景下对cdc2氨酸酸化状态的分析.
主要成果:
- Mik1与Wee1有冗余的作用,对cdc2.2.进行负调节.
- 一个mik1 wee1的双重突变体表现出高甲状腺致死性,绕过关键的M阶段检查点.
- 缺少Mik1和Wee1导致cdc2氨酸的快速脱.
结论:
- Mik1和Wee1在抑制cdc2.2.的氨酸酸化中进行合作.
- 这些激酶对于保持M相完整性和检查点控制至关重要.
- 这些发现表明Mik1和Wee1要么是直接的抑制性激酶,要么是cdc2.2的抑制性激酶的基本激活剂.
相关概念视频
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