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人类ADAR1防止内源RNA触发转化关闭

Hachung Chung¹, Jorg J A Calis², Xianfang Wu¹

¹Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, NY 10065, USA.

|February 4, 2018

概括

酶ADAR1通过编辑双链RNA (dsRNA) 来阻止自身RNA引发免疫反应. ADAR1淘汰细胞表现出自发的干扰素产生,突出其在区分自我与非自我核酸中的作用.

科学领域:

免疫学
分子生物学
遗传学

背景情况:

I型干扰素 (IFN) 的产生是由检测外来核酸的宿主传感器触发的.
这些传感器区分自我与非自我双链RNA (dsRNA) 的机制尚不清楚.
编辑dRNA的ADAR1酶的突变与艾卡迪-古蒂耶综合征有关,这种综合征的特征是自身炎症和神经问题.

研究的目的:

研究ADAR1在人类细胞中的基质和功能.
了解ADAR1如何区分自我与非自我核酸.
阐明ADAR1在调节干扰素反应和预防自身炎症中的作用.

主要方法:

为功能研究生成ADAR1淘汰人类细胞.
分析了RNA聚合酶II (pol II) 和pol III转录中的ADAR1编辑活性.
评估了ADAR1对IFN反应中的PKR激活和转化关闭的影响.
研究了ADAR1在神经元前体细胞中MDA5依赖的干扰素的作用.

主要成果:

ADAR1主要编辑了pol II转录的mRNA中的Alu元素,而不是pol III转录的Alus.
ADAR1 抑制了 dsRNA 传感器 PKR 的过度激活,防止了 IFN 反应期间的转化关闭.
为了防止内源RNA激活PKR,ADAR1的dSRNA结合和催化活动都至关重要.
发生自发的MDA5依赖性干扰素产生,PKR激活和细胞死亡.

结论:

人类ADAR1在调节自我与非自我RNA的感知方面发挥着关键作用.
通过ADAR1可以检测病原体,同时防止有害的自身炎症反应.
通过降低自身RNA耐受性,ADAR1的失调会导致自身炎症.

关键词:

一个ADAR1 一个 AGS 艾卡迪-古提耶氏综合征元素其他国家在PKR 编辑RNA 天生的免疫力神经元前代细胞翻译一种类型的干扰素

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