在因细胞循环负控制基因突变阻断的细胞中,螺纹形成和染色质凝聚
S A Osmani1, D B Engle, J H Doonan
1Department of Pharmacology, Robert Wood Johnson Medical School, UMDNJ, Piscataway 08854.
Cell
|January 29, 1988
概括
Aspergillus nidulans bimE7突变引发过早的线粒分裂,在S或G2阶段导致染色体凝聚和螺旋体形成. 这种功能丧失突变取代了细胞周期控制,这表明bime负面调节了线粒体的进入.
科学领域:
- 细胞生物学 细胞生物学
- 分子遗传学 分子遗传学
- 菌类遗传学 菌类遗传学
背景情况:
- 细胞循环通过DNA复制和线粒分裂来确保有序的进展.
- 对温度敏感的突变,比如阿斯伯吉路斯尼杜兰斯中的bimE7,允许研究人员在特定条件下研究必要的基因.
- 过早进入线粒分裂可以破坏基因组的完整性.
研究的目的:
- 研究BIME基因在细胞循环调节中的功能.
- 为了确定bimE7突变是否绕过正常细胞周期检查点.
- 阐明bime在控制线粒分裂的开始中的作用.
主要方法:
- 在bimE7和S/G2阶段突变之间构建双重突变.
- 细胞循环的同步使用基尿素来阻止DNA复制.
- 微观分析染色体凝聚和阿斯伯吉路斯尼杜兰斯中螺旋的形成.
主要成果:
- 双E7突变诱导了在S或G2阶段被捕的细胞中的染色体凝聚和形形成.
- 这种过早的线粒事件发生在DNA复制被阻断时.
- bimE7被证实是一种功能丧失突变.
结论:
- 双E7突变覆盖了细胞周期控制系统,这些系统通常会防止过早的线粒分裂.
- 双E基因可能会作为一个积极的线粒诱导物的负调节器,可能是nimA基因.
- 了解bimE的功能,可以了解在DNA复制或修复过程中防止线粒体进入的机制.
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