信使核糖核酸
细胞生物学
生物
化学
基因
遗传学
作者
Soo Seok Hwang,Jaechul Lim,Zhibin Yu,Philip Kong,Esen Sefik,Hao Xu,Christian C. D. Harman,Lark Kyun Kim,Gap Ryol Lee,Huabing Li,Richard A. Flavell
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2020-03-12
卷期号:367 (6483): 1255-1260
被引量:205
标识
DOI:10.1126/science.aax0194
摘要
T cells maintain a quiescent state prior to activation. As inappropriate T cell activation can cause disease, T cell quiescence must be preserved. Despite its importance, the mechanisms underlying the "quiescent state" remain elusive. Here, we identify BTG1 and BTG2 (BTG1/2) as factors responsible for T cell quiescence. BTG1/2-deficient T cells show an increased proliferation and spontaneous activation due to a global increase in messenger RNA (mRNA) abundance, which reduces the threshold to activation. BTG1/2 deficiency leads to an increase in polyadenylate tail length, resulting in a greater mRNA half-life. Thus, BTG1/2 promote the deadenylation and degradation of mRNA to secure T cell quiescence. Our study reveals a key mechanism underlying T cell quiescence and suggests that low mRNA abundance is a crucial feature for maintaining quiescence.
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