期刊
SCIENCE
卷 367, 期 6483, 页码 1255-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax0194
关键词
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资金
- Howard Hughes Medical Institute
- Leslie H. Warner Fellowship from Yale Cancer Center (YCC)
- HFSPO [LT000037/2018-L]
- Jane Coffin Childs Memorial Fund
- National Research Foundation of Korea [NRF-2017R1A2B3008621]
- National Natural Science Foundation of China [91753141]
- Shanghai Jiao Tong University School of Medicine
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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