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DDX54驱动ALKBH5介导的选择转录的脱甲基化,以抑制干扰素的抗病毒反应

Hao-Yu Sun^1,2, Xiu-Ying Gong^1,2, Zi-Ling Qu^1,2

¹Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, China.

Journal of virology

|August 12, 2025

概括

死亡盒化酶54 (DDX54) 通过促进m6A转录的脱甲基化来抑制I型干扰素的抗病毒反应. 这种机制涉及DDX54与ALKBH5相互作用,在病毒感染期间损害宿主抗病毒信号.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
病毒学病毒学

背景情况:

死亡盒 (DDX) 蛋白通过对抗病毒信号转录的N⁶-methyladenosine (m⁶A) 修改来调节天生的免疫力.
单个DDX蛋白在抗病毒反应中的特定作用仍然在很大程度上是未知的.

研究的目的:

为了确定参与抗病毒反应的特定DDX蛋白质.
阐明DDX54调节I型干扰素抗病毒反应的机制.

主要方法:

使用VSV感染模型研究DDX54在干扰素抗病毒反应中的作用.
使用了DDX54和ALKBH5.5的淘汰和淘汰策略.
分析了转录本地化,m⁶A修改状态,以及蛋白质-蛋白质相互作用.

主要成果:

过度表达DDX54抑制了干扰素反应并促进了VSV复制;DDX54的耗尽具有相反的效果.
DDX54通过ALKBH5.6促进特定转录物的去甲基化,包括mRNA,通过ALKBH5.
VSV感染诱导DDX54转移到核质中,在那里它增强ALKBH5对目标转录的活性,限制它们的翻译和损害抗病毒防御.

结论:

DDX54作为I型干扰素抗病毒反应的抑制剂.
在VSV感染期间,DDX54/m6/A/ALKBH5轴被激活,以微调宿主抗病毒免疫力.
DDX54的ATPase活性对于其与转录的相互作用和增强ALKBH5脱甲基酶活性至关重要.

关键词:

在 ALKBH5H5 中死亡盒螺旋酶 54 在死亡盒中.脱甲基化活动.干扰素的反应是干扰素的反应.基质选择性基质选择性

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