移除Intron需要校对DEK对U2AF/3'拼接部位识别的校对
Luis Miguel Mendes Soares1, Katia Zanier, Cameron Mackereth
1Centre de Regulació Genòmica, Passeig Marítim 37-49, 08003 Barcelona, Spain.
Science (New York, N.Y.)
|July 1, 2006
概括
蛋白DEK,当化时,通过确保拼接因子U2AF正确识别3'拼接位,有助于精确的内子去除. 这种校对机制对于真核生物中信使RNA的形成至关重要.
科学领域:
- 分子生物学分子生物学
- 在RNA分离过程中.
- 癌症生物学 癌症生物学
背景情况:
- 精确的内子去除和信使RNA形成取决于区分从类似的序列拼接站点.
- 由U2AF65和U2AF35子单元组成的拼接因子U2AF识别了metazoan 3'拼接位的关键元素.
- 已知涉及某些癌症的DEK蛋白与染色质和RNA有关.
研究的目的:
- 研究DEK蛋白在3'拼接部位识别中的作用,由U2AF.
- 阐明DEK影响拼接部位歧视的机制.
- 为了确定DEK化对U2AF结合和内离子去除的影响.
主要方法:
- 同免疫沉以评估蛋白质相互作用.
- 在体外结合测试以研究U2AF亚单元与拼接部位元素的相互作用.
- 在DEK及其酸化形式的存在和缺席下分析RNA拼接效率.
主要成果:
- 化DEK (在19和32序列) 与U2AF35.35相关.
- DEK促进了U2AF35和在3'拼接部位保存的AG二核酸之间的相互作用.
- DEK防止U2AF65与AG不遵循的金胺通道结合,从而提高拼接位的保真度.
- DEK及其酸化对于内部去除是必不可少的,但对于拼接复合物的初始组装不是.
结论:
- 德克作为一个关键的监管者,对U2AF的3'拼接部位歧视.
- DEK的酸化对于其促进准确的拼接部位识别的功能至关重要.
- 这一由DEK调解的早期校对步骤影响了结合体的催化激活,影响了整体的拼接效率.
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