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mRNA destabilization by BTG1 and BTG2 maintains T cell quiescence

Cited 94 time in Web of Science Cited 102 time in Scopus

Hwang, Soo Seok; Lim, Jaechul; Yu, Zhibin; Kong, Philip; Sefik, Esen; Xu, Hao; Harman, Christian C. D.; Kim, Lark Kyun; Lee, Gap Ryol; Li, Hua-Bing; Flavell, Richard A.

Issue Date
American Association for the Advancement of Science
Science, Vol.367 No.6483, pp.1255-+
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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  • College of Veterinary Medicine
  • Department of Veterinary Medicine
Research Area Extreme stress, Local glucocorticoids, Stress adaptation


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