口通过刺激暂停的RNA聚合酶II释放来诱导转录
Julia M Rogers1, Claudia A Mimoso1, Benjamin Je Martin1
1Department of Biological Chemistry and Molecular Pharmacology, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
bioRxiv : the preprint server for biology
|June 25, 2024
概括
缺口信号通过释放暂停的RNA聚合酶II (RNAPII) 来激活目标基因,而不是通过增加染色质可访问性来激活. 预先存在的染色质状态决定了对Notch激活的核反应.
科学领域:
- 分子生物学分子生物学
- 细胞信号传输 细胞信号传输
- 基因规则 基因规则
背景情况:
- 划分蛋白是通过转录控制细胞过程的关键调节者.
- 诺奇信号诱导目标基因转录的确切机制尚不完全理解.
研究的目的:
- 阐明 Notch1 诱导的基因转录的分子机制.
- 调查染色质可访问性和RNA聚合酶II动态在Notch信号传递中的作用.
主要方法:
- 使用高分辨率的基因组测试来分析染色质可访问性.
- 新生的RNA产量被测量在人类Notch1激活的时间过程中.
主要成果:
- 痕信号主要通过释放暂停的RNA聚合酶II (RNAPII) 来诱导转录.
- 在通过SWI/SNF重塑的Notch信号诱导之前,已经确定了调节元件的染色质可访问性.
- 预先存在的染色质状态和RNAPII分布决定了对Notch信号的核反应.
结论:
- 缺口诱导的转录依赖于暂停RNAPII的释放.
- 目前存在的Notch信号模型需要修改,强调先前存在的染色质状态,而不是Notch诱导的可访问性变化.
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