通过Maf1抑制RNA聚合酶III转录的分子基础
Alessandro Vannini1, Rieke Ringel, Anselm G Kusser
1Gene Center and Department of Biochemistry, Center for Integrated Protein Science Munich (CIPSM), Ludwig-Maximilians-Universität München, Feodor-Lynen-Strasse 25, 81377 Munich, Germany.
Cell
|October 5, 2010
概括
蛋白Maf1抑制在压力下RNA聚合酶III (Pol III) 的转录启动. 结构研究表明,Maf1与Pol III结合,防止基本因子的招募和停止转录.
科学领域:
- 分子生物学分子生物学
- 结构生物学 结构生物学
- 生物化学 生物化学
背景情况:
- RNA聚合酶III (Pol III) 对于转录细胞功能至关重要的短RNA至关重要.
- 蛋白质Maf1是Pol III转录的保存抑制剂,特别是在压力条件下.
研究的目的:
- 阐明Maf1抑制Pol III转录的结构机制.
- 了解Maf1如何与Pol III相互作用并影响转录启动过程.
主要方法:
- 进行X射线晶体学以确定Maf1.1的结构.
- 低温电子显微镜可视化Pol III,活跃的Pol III-DNA-RNA复合体,以及压制性的Pol III-Maf1复合体.
主要成果:
- 结合DNA和RNA会诱导Pol III特异性C82/34/31亚复合物的排序,这对于转录启动至关重要.
- Maf1与Pol III结,重新定位C82/34/31亚复合体,并阻碍Pol III对促进DNA和启动因子的招募.
- Maf1结合可以防止封闭复合体的形成,但不会抑制DNA-RNA支架结合或RNA合成.
结论:
- Maf1通过干扰预启动复合体的组装来特别抑制Pol III转录启动.
- Maf1与Pol III的结合似乎也可以防止在延长过程中转录的重新启动.
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