RNA聚合酶III转录相关的多基解促进了感染期间非编码逆转移子的积累
bioRxiv : the preprint server for biology
|June 4, 2025
概括
病毒感染通过增加RNA聚合酶III转录和招募多基化机制来调节短间隔核元素 (SINE) RNA. 这一过程稳定了SINERNAs,在致病性压力期间增加了它们的丰富性.
科学领域:
- 分子生物学分子生物学
- 病毒学 病毒学
- 基因组学就是基因组学.
背景情况:
- 短间隔核元素 (SINEs) 是RNA聚合酶III (Pol III) 转录的逆转移子.
- SINE RNA积累是细胞压力的标志,包括病毒感染.
- 在感染期间驱动SINE诱导的机制尚不清楚.
研究的目的:
- 为了阐明SINERNA诱导在gammaherpesvirus感染期间的分子机制.
- 确定涉及到SINERNAs稳定的主要特征和途径.
主要方法:
- 开发了一个基于卷积神经网络 (CNN) 的模型来识别SINE特征.
- 利用基因组学分析来研究SINE RNA处理和积累.
- 研究了mRNA多基化机制对Pol III转录的位置的招募.
主要成果:
- 确定了与多基化相关的基因作为感染诱导的SINEs的关键标志.
- 证明了氏体病毒感染诱导mRNA类3'端处理SINERNAs.
- 显示了多基化机制被招募到SINE和tRNA基因以一种Pol III-依赖的方式.
- 证实SINE ncRNA增强的多基解是必要的,以便在感染期间稳定积累.
结论:
- 氏体病毒感染将Pol III转录与mRNA类似的多基化结合起来,用于SINE RNA稳定.
- 在病原性压力期间,Pol III对多基化机制的选择增加了非编码RNA的丰富性.
- 在压力期间,Pol III转录3'末端处理中的诱导性改变调节非编码的逆转移素丰度.
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