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通过ADAR1编辑RNA,防止MDA5感知内源的dsRNA为非自身

Brian J Liddicoat¹, Robert Piskol², Alistair M Chalk¹

¹St. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia. Department of Medicine, St. Vincent's Hospital, University of Melbourne, Fitzroy, Victoria 3065, Australia.

Science (New York, N.Y.)

|August 15, 2015

概括

通过ADAR1编辑氨酸到氨酸对于预防胚胎死亡至关重要. 这种RNA编辑防止内源转录激活双链RNA (dsRNA) 传感途径.

科学领域:

分子生物学
遗传学
免疫学

背景情况:

氨酸到氨酸 (A-to-I) 编辑是关键的RNA修改.
通过ADAR (作用于RNA的腺氨酸脱氨酶) 酶进行A-to-I编辑.
ADAR1已经提出了超越RNA编辑的功能.

研究的目的:

阐明ADAR1介导的RNA编辑的重要作用.
研究ADAR1的体内基质和功能.
确定ADAR1的基本功能是编辑RNA.

主要方法:

产生具有编辑缺陷ADAR1突变的小鼠 (Adar1 ((E861A/E861A)).
分析胚胎死亡率和干扰素/dsRNA感应通路的激活.
进行全基因组分析以确定ADAR1基质.
通过删除 dsRNA 传感器 MDA5 来评估救援表型.

主要成果:

亚达1 (E861A/E861A) 胚胎的胚胎死亡率在E13.5左右.
在突变胚胎中观察到激活的干扰素和dRNA感应通路.
全基因组分析显示了内源转录的dsRNA干循环中的超编辑.
同时删除 MDA5 挽救的胚胎死亡率和表型.

结论:

ADAR1的主要功能是内源dRNA的A-to-I编辑.
这种编辑阻止了细胞核dRNA反应的激活.
通过编辑内生dRNA,ADAR1作为先天免疫的关键调节者.

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