在热冲击后,CPSF73激活和3'RNA聚合酶II暂停在读透转录期间丢失
Kaitlyn E Walsh1, James A Goodrich1, Jennifer F Kugel1
1Department of Biochemistry, University of Colorado, Boulder, CO 80309, USA.
Cell reports
|February 27, 2026
概括
热冲击导致RNA聚合酶II (Pol II) 转录过去的基因结尾. 这种读透转录与改变的Pol II速度,C端域 (CTD) 酸化和CPSF73活性有关,涉及RBBP6.
科学领域:
- 分子生物学分子生物学
- 基因表达规范 基因表达规范
- 细胞应激反应的应激反应
背景情况:
- 环境压力会破坏正常的基因表达.
- RNA聚合酶II (Pol II) 通常会在mRNA基因的特定部位中终止转录.
- 波尔二号绕过处于压力状态的终端站点的机制尚未完全理解.
研究的目的:
- 调查热冲击期间Pol II读透转录背后的分子机制.
- 识别转录终结变化的因素和修改.
- 阐明CPSF73和RBBP6在压力诱导的读透转录中的作用.
主要方法:
- 在热冲击处理后对Pol II转录模式的分析.
- 对Pol II C终端域 (CTD) 酸化的评估.
- 研究3'基因末端的内核分解裂变活性.
- 在热冲击期间的基因表达操纵 (RBBP6的过度表达).
主要成果:
- 热冲击诱导了成千上万个基因下游的显著读透转录.
- 在基因3'结束后的Pol II暂停在热冲击后被废除.
- 在Pol II CTD中观察到Tyr1和Ser2酸化的增加,但在读透基因时减弱.
- 终止至关重要的内核分裂裂变在读透基因方面有缺陷.
- 过度表达RBBP6可以挽救分离缺陷,并减少读透转录.
结论:
- 热冲击触发了一种多方面的机制,涉及改变的Pol II速度,CTD酸化和CPSF73活性.
- RBBP6在调节CPSF73活动和减轻压力诱导的读透转录方面发挥作用.
- 这些发现提供了关于细胞如何在环境压力下适应基因表达的见解.
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