Homo sapiens Targeted loci cultured

The exosome-independent exoribonuclease DIS3L2 is mutated in Perlman syndrome.Using 3'' RACE-Seq, we demonstrate that all novel DIS3L2 substrates areuridylated in vivo by TUT4/TUT7 poly(U) polymerases. Uridylation-dependent DIS3L2-mediated decay can be recapitulated in vitro, thus reinforcing the tight cooperationbetween DIS3L2 and TUTases.不依赖外切酶体的外切核糖核酸酶DIS3L2（exosome-independent exoribonuclease DIS3L2）的突变可引发珀尔曼综合征。本研究采用3'末端快速扩增测序（3'' RACE-Seq）技术，证实所有新鉴定的DIS3L2底物在体内均可被TUT4/TUT7多聚尿苷酸聚合酶（TUT4/TUT7 poly(U) polymerases）介导尿苷酸化修饰。依赖尿苷酸化的DIS3L2介导的降解过程可在体外重现，这进一步强化了DIS3L2与TUT酶之间的紧密协同作用。