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mRNA Destabilization by BTG1 and BTG2 Maintains T Cell Quiescence

Authors
 Soo Seok Hwang  ;  Jaechul Lim  ;  Zhibin Yu  ;  Philip Kong  ;  Esen Sefik  ;  Hao Xu  ;  Christian C D Harman  ;  Lark Kyun Kim  ;  Gap Ryol Lee  ;  Hua-Bing Li  ;  Richard A Flavell 
Citation
 SCIENCE, Vol.367(6483) : 1255-1260, 2020-03 
Journal Title
 SCIENCE 
ISSN
 0036-8075 
Issue Date
2020-03
MeSH
Animals ; Cells, Cultured ; Immediate-Early Proteins / genetics ; Immediate-Early Proteins / physiology* ; Lymphocyte Activation* ; Mice ; Mice, Knockout ; Neoplasm Proteins / genetics ; Neoplasm Proteins / physiology* ; Polyadenylation ; RNA Stability* ; RNA, Messenger / chemistry* ; T-Lymphocytes / immunology* ; Tumor Suppressor Proteins / genetics ; Tumor Suppressor Proteins / physiology*
Abstract
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.
Full Text
https://science.sciencemag.org/content/367/6483/1255.long
DOI
10.1126/science.aax0194
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Kim, Lark Kyun(김락균) ORCID logo https://orcid.org/0000-0001-5983-4470
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/176078
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