Wu Guowei, Radwan Mohamed K, Xiao Mu, Adachi Hironori, Fan Jason, Yu Yi-Tao
Department of Biochemistry and Biophysics, Center for RNA Biology, University of Rochester Medical Center, Rochester, New York 14642, USA.
RNA. 2016 Aug;22(8):1146-52. doi: 10.1261/rna.056796.116. Epub 2016 Jun 7.
Pseudouridine (Ψ) has been identified in various types of RNAs, including mRNA, rRNA, tRNA, snRNA, and many other noncoding RNAs. We have previously shown that RNA pseudouridylation, like DNA and protein modifications, can be induced by stress. For instance, growing yeast cells to saturation induces the formation of Ψ93 in U2 snRNA. Here, we further investigate this inducible RNA modification. We show that switching yeast cells from nutrient-rich medium to different nutrient-deprived media (including water) results in the formation of Ψ93 in U2 snRNA. Using gene deletion/conditional depletion as well as rapamycin treatment, we further show that the TOR signaling pathway, which controls cell entry into stationary phase, regulates Ψ93 formation. The RAS/cAMP signaling pathway, which parallels the TOR pathway, plays no role in this inducible modification.
假尿苷(Ψ)已在多种类型的RNA中被鉴定出来,包括信使核糖核酸(mRNA)、核糖体核糖核酸(rRNA)、转运核糖核酸(tRNA)、小核核糖核酸(snRNA)以及许多其他非编码RNA。我们之前已经表明,RNA假尿苷化,如同DNA和蛋白质修饰一样,可由应激诱导产生。例如,将生长中的酵母细胞培养至饱和状态会诱导U2小核核糖核酸中Ψ93的形成。在此,我们进一步研究这种可诱导的RNA修饰。我们发现,将酵母细胞从营养丰富的培养基转移至不同的营养缺乏培养基(包括水)会导致U2小核核糖核酸中Ψ93的形成。通过基因缺失/条件性缺失以及雷帕霉素处理,我们进一步表明,控制细胞进入静止期的TOR信号通路调节Ψ93的形成。与TOR通路平行的RAS/环磷酸腺苷(cAMP)信号通路在这种可诱导修饰中不起作用。