Hüttenhofer A, Weiss-Brummer B, Dirheimer G, Martin R P
Institut de Biologie Moléculaire et Cellulaire du CNRS, Laboratoire de Biochimie, Strasbourg, France.
EMBO J. 1990 Feb;9(2):551-8. doi: 10.1002/j.1460-2075.1990.tb08142.x.
We have identified a spontaneous mitochondrial mutation, mfs-1 (mitochondrial frameshift suppressor-1), which suppresses a + 1 frameshift mutation localized in the yeast mitochondrial oxi1 gene. The suppressor strain exhibits a single base change (C to U) at position 42 of the mitochondrial serine-tRNA (UCN). To our knowledge, this is the first reported case showing that a mutation in the anticodon stem of a tRNA can cause frameshift suppression. The expression and aminoacylation of the mutant tRNASer(UCN) are not significantly affected. However, the base change at position 42 has two effects: first, residue U27 of the mutant tRNA is not modified to pseudouridine as observed in wild-type tRNASer(UCN). Second, the base change and/or the lack of modification of U27 leads to an alteration in the secondary/tertiary structure of the mutant tRNA. It is possible that there are such structural changes in the anticodon loop that enable the tRNA to read a four base codon, UCCA, thus restoring the wild-type reading frame.
我们鉴定出一种自发的线粒体突变，即mfs-1（线粒体移码抑制因子-1），它能抑制位于酵母线粒体oxi1基因中的一个+1移码突变。该抑制菌株在线粒体丝氨酸-tRNA（UCN）的第42位出现了一个单碱基变化（从C到U）。据我们所知，这是首次报道的表明tRNA反密码子茎中的突变可导致移码抑制的案例。突变型tRNASer(UCN)的表达和氨酰化未受到显著影响。然而，第42位的碱基变化有两个影响：第一，与野生型tRNASer(UCN)不同，突变型tRNA的U27残基未被修饰为假尿苷。第二，碱基变化和/或U27缺乏修饰导致突变型tRNA的二级/三级结构发生改变。反密码子环中可能存在这样的结构变化，使tRNA能够读取四碱基密码子UCCA，从而恢复野生型阅读框。
