复制的链接由Cdk抑制剂Sic1开始
B L Schneider1, Q H Yang, A B Futcher
1Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
Science (New York, N.Y.)
|April 26, 1996
概括
该研究表明,Sic1无活化是酵母细胞分裂中G1环林 (Clns) 的关键作用. 通过Clns对Sic1的酸化和降解调节了Start过渡时的DNA复制承诺.
科学领域:
- 细胞生物学 细胞生物学
- 分子生物学分子生物学
- 酵母遗传学 酵母遗传学
背景情况:
- 三种G1循环蛋白 (Clns) 调节Saccharomyces cerevisiae中的启动事件,使细胞进行分裂.
- Sic1是已知的C1b-Cdc28激酶的抑制剂,对细胞周期进展至关重要.
研究的目的:
- 阐明G1环林 (Clns) 在酵母细胞分裂中的基本功能.
- 调查Sic1酸化和降解在Start过渡中的作用.
主要方法:
- 对缺乏特定环林和Sic1.1的Saccharomyces cerevisiae突变物的分析.
- 研究与ClN活性相关的Sic1的酸化和降解.
主要成果:
- 开始时的Sic1酸化取决于Cln活动.
- 在Sic1降解过程中,需要Clns和ubiquitin结合酶Cdc34.
- Sic1 失活是 Clns 的唯一非冗余的基本功能,因为 sic1 删除拯救了 cln1 cln2 cln3 三重突变.
- sic1突变体表现出未合的DNA复制和芽.
结论:
- Sic1是Cln-Cdc28复合物的可能基质.
- 酸化和随后的Clns对Sic1的蛋白质分解对于调节在Start过渡时对DNA复制的承诺至关重要.
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