한빛사 논문
Jaechul Lim,1,2,4 Minju Ha,1,2,4 Hyeshik Chang,1,2,4 S. Chul Kwon,1,2 Dhirendra K. Simanshu,3 Dinshaw J. Patel,3 and V. Narry Kim1,2,*
1Center for RNA Research, Institute for Basic Science, Seoul 151-742, Korea
2School of Biological Sciences, Seoul National University, Seoul 151-742, Korea
3Structural Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA
4Co-first author
*Correspondence: V. Narry Kim
Abstract
Uridylation occurs pervasively on mRNAs, yet its mechanism and significance remain unknown. By applying TAIL-seq, we identify TUT4 and TUT7 (TUT4/7), also known as ZCCHC11 and ZCCHC6, respectively, as mRNA uridylation enzymes. Uridylation readily occurs on deadenylated mRNAs in cells. Consistently, purified TUT4/7 selectively recognize and uridylate RNAs with short A-tails (less than ∼25 nt) in vitro. PABPC1 antagonizes uridylation of polyadenylated mRNAs, contributing to the specificity for short A-tails. In cells depleted of TUT4/7, the vast majority of mRNAs lose the oligo-U-tails, and their half-lives are extended. Suppression of mRNA decay factors leads to the accumulation of oligo-uridylated mRNAs. In line with this, microRNA induces uridylation of its targets, and TUT4/7 are required for enhanced decay of microRNA targets. Our study explains the mechanism underlying selective uridylation of deadenylated mRNAs and demonstrates a fundamental role of oligo-U-tail as a molecular mark for global mRNA decay.
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