Zhuravleva G A, Gryzina V A
Mol Biol (Mosk). 2012 Mar-Apr;46(2):285-97.
Eukaryotic cells possess special mechanism of the degradation of mRNAs containing premature termination codons (PTCs)--nonsense-mediated mRNA decay (NMD) pathway. In yeast Saccharomyces cerevisiae, the activity of this pathway depends on the recognition of the PTC by the translational machinery and interaction of translation termination factors eRF1 and eRF3 with Upf1, Upf2 and Upf3 proteins. Previously we have shown that decreasing of eRF1 amount causes an impairment of NMD. Here we show that deletion of either UPF1 or UPF2 increased viability of sup45 mutants, while effect of UPF3 deletion is allele-specific. Two-hybrid data have shown that aa 1-555 of eRF1 participate in interaction with Upf1. Deletion of each UPF gene leads to allosuppresson of ade1-14 mutation without changing eRF1 amount. Depletion of Upf1 does not influence synthetic lethality of sup45 and prion [PSI+]. It is possible that the absence of Upf1 (or its activator Upf2) leads to more effective formation of the translation termination complex and, consequently, increased viability of cells containing mutant termination factors.
真核细胞拥有一种特殊机制，用于降解含有提前终止密码子（PTC）的mRNA——无义介导的mRNA降解（NMD）途径。在酿酒酵母中，该途径的活性取决于翻译机器对PTC的识别以及翻译终止因子eRF1和eRF3与Upf1、Upf2和Upf3蛋白的相互作用。此前我们已经表明，eRF1数量的减少会导致NMD受损。在此我们表明，缺失UPF1或UPF2会增加sup45突变体的存活率，而缺失UPF3的影响具有等位基因特异性。双杂交数据表明，eRF1的第1至555个氨基酸参与与Upf1的相互作用。每个UPF基因的缺失都会导致ade1 - 14突变的异源抑制，而不改变eRF1的数量。缺失Upf1不会影响sup45和朊病毒[PSI+]的合成致死性。有可能缺失Upf1（或其激活剂Upf2）会导致翻译终止复合物更有效地形成，从而提高含有突变终止因子的细胞的存活率。
