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METTL16通过调节S-adenosylmethionine循环来控制卡波西肉瘤相关的疹病毒复制

Xinquan Zhang^1,2, Wen Meng^1,2, Jian Feng^1,2

¹Cancer Virology Program, University of Pittsburgh Medical Center Hillman Cancer Center, Pittsburgh, PA, USA.

Cell death & disease

|September 6, 2023

概括

通过调节SAM循环和细胞氧化应激,METTL16抑制了卡波西肉瘤相关性疹病毒 (KSHV) 的溶性复制. 这种RNA甲基转移酶通过影响代谢和氧化还原条件,影响KSHV病变发生.

科学领域:

病毒学病毒学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

卡波西的肉瘤相关性疹病毒 (KSHV) 具有潜伏和溶性复制阶段,对于癌症的发展至关重要.
N6-甲基氨酸 (m6A) 修改调节了KSHV生命周期.
METTL16在KSHV复制中的作用以前是未知的.

研究的目的:

研究METTL16在KSHV生命周期中的功能.
阐明METTL16影响KSHV复制的分子机制.

主要方法:

基因淘汰和METTL16的过度表达.
分析KSHV光学复制的分析.
对MAT2A拼接和表达的评估.
测量细胞内S-adenosylmethionine (SAM) 的水平. 在细胞内测量S-adenosylmethionine (SAM) 的水平.
评估活性氧物种 (ROS) 和谷氨水平.

主要成果:

METTL16敲除增强了KSHV的Lytic复制;过度表达抑制了它.
METTL16调节MAT2A的m6A修改,影响其表达.
MAT2A抑制或淘汰降低了SAM水平,并增强了KSHV的溶性复制.
补充SAM可以抑制KSHV的溶性复制,并逆转METTL16/MAT2A的淘汰效应.
METTL16/MAT2A调制改变了细胞内ROS和谷氨水平,影响了KSHV复制.

结论:

METTL16通过调节SAM循环并维持氧化还原平衡来抑制KSHV的溶性复制.
该研究将KSHV生命周期与特定的m6A修饰和细胞代谢/氧化状态联系起来.
METTL16代表了治疗干预KSHV相关疾病的潜在目标.

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