通过Cdc5和细胞循环检查点对Bub2/Bfa1 GAP复合物的调节
1Verna and Mars McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.
Cell
|December 6, 2001
概括
波罗/Cdc5激酶对抗Bfa1/Bub2以促进线粒体的退出. 细胞循环检查点调节Bfa1酸化,确保在发生DNA损伤时进行线粒离子停止.
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:
- 1GTPase通过信号传导途径启动了线粒体的退出.
- 在细胞周期的大部分时间里,Bfa1/Bub2复合体对抗Tem1功能.
- 对于Bfa1/Bub2复合体的调节还没有完全理解.
研究的目的:
- 为了调查Bfa1/Bub2复合体的上游调节器.
- 阐明Bfa1/Bub2是如何通过细胞周期检查点控制的.
- 了解Polo/Cdc5激酶在线粒体退出网络中的作用.
主要方法:
- 研究了Polo/Cdc5激酶和Bfa1/Bub2.2之间的相互作用.
- 分析了Cdc5对Bfa1酸化的影响.
- 通过线组件和线方向检查点检查的Bfa1调节.
- 研究了DNA损伤对通过Rad53和Dun1.1修改Bfa1的影响.
主要成果:
- 波罗/Cdc5激酶酸化Bfa1,对抗其功能并促进线粒体的退出.
- 线组件和线定向检查点可以抑制Bfa1酸化.
- DNA损伤诱导了Bfa1的Rad53-和Dun1-依赖的修饰,独立于抑制酸化.
- 通过Cdc5和检查点调节Bfa1对于确保线粒体的停止至关重要.
结论:
- 波罗/Cdc5激酶是线粒离出路中Bfa1/Bub2的上游调节者.
- 细胞周期检查点和DNA损伤对Bfa1酸化进行差异调节.
- 通过多个途径修改Bfa1是确保适当的线粒体停止的关键机制.
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