Regulation of deadenylation and its role in T cell quiescence

  • Hit 522
  • Writer 최고관리자
  • 2019-07-11


[BK21 Plus Seminar]

▶Subject: Regulation of deadenylation and its role in T cell quiescence

▶Speaker: Jaechul Lim, D.V.M., Ph.D. (Department of Immunobiology, Yale University School of Medicine)


▶Date: 4:30 PM/July 23(Tue.)/2019


▶Place: Auditorium(1F), Postech Biotech Center

messenger RNA (mRNA) plays central roles in the delivery of genetic information. Posttranscriptional modifications of mRNA, such as poly(A) tailing, greatly affect mRNA translation and stability. Recently, we discovered mixed tailing of poly(A) tail, a novel mRNA modification, which expands the complexity of posttranscriptional gene regulation. We found that intermittent non-adenosine residues are generated by TENT4A and TENT4B and shield mRNA from rapid deadenylation.
Today, I will present how deadenylation promotes mRNA turnover to maintain T cell quiescence. We identify BTG1 and BTG2 (BTG1/2) as novel factors responsible for T cell quiescence. BTG1/2 deficiency in T cells resulted in an increased proliferation and spontaneous activation of naive T cells. We found a global increase in mRNA abundance in the absence of BTG1/2, which reduced threshold to activation. Depletion of BTG1/2 led to an increase in poly(A) tail length, leading to a greater mRNA half-life in naive T cells. Thus, BTG1/2 promotes deadenylation and degradation of mRNA to secure T cell quiescence. Our study demonstrates a key mechanism underlying T cell quiescence, and suggests low mRNA abundance as a crucial feature for maintaining the quiescent state.


▶Inquiry: Prof. Yoontae Lee (279-2354)


 * This seminar will be given in English.
  Please refrain from taking photos during seminars. *