The translational decoding properties of tRNAs are influenced by post-transcriptional modification of nucleosides in their anticodon region. The Elongator complex promotes the first step in the formation of 5-methoxycarbonylmethyl (mcm5), 5-methoxycarbonylhydroxymethyl (mchm5), and 5-carbamoylmethyl (ncm5) groups on wobble uridine residues in eukaryotic cytosolic tRNAs. Elongator mutants in yeast, worms, plants, mice, and humans not only show a tRNA modification defect, but also a diverse range of additional phenotypes. Even though the phenotypes are almost certainly caused by the reduced functionality of the hypomodified tRNAs in translation, the basis for specific phenotypes is not well understood. Here, we discuss the recent finding that the phenotypes of Saccharomyces cerevisiae Elongator mutants are modulated by the genetic background. This background-effect is largely due to the allelic variation at the SSD1 locus, which encodes an mRNA-binding protein involved in post-transcriptional regulation of gene expression. A nonsense ssd1 allele is found in several wild-type laboratory strains and the presence of this allele aggravates the stress-induced phenotypes of Elongator mutants. Moreover, other phenotypes, such as the histone acetylation and telomeric gene silencing defects, are dependent on the mutant ssd1 allele. Thus, SSD1 is a genetic modifier of the phenotypes of Elongator-deficient yeast cells.

中文翻译：

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SSD1修改了Elongator突变体的表型。

tRNA的翻译解码特性受其反密码子区域中核苷的转录后修饰的影响。Elongator复合物促进了真核细胞质tRNA中摆动尿苷残基上形成5-甲氧基羰基甲基（mcm5），5-甲氧基羰基羟甲基（mchm5）和5-氨基甲酰基甲基（ncm5）基团的第一步。酵母，蠕虫，植物，小鼠和人类中的延伸子突变体不仅显示出tRNA修饰缺陷，而且还表现出多种多样的其他表型。即使表型几乎可以肯定是由于翻译中低修饰的tRNA的功能降低所致，但对特定表型的依据尚不甚了解。在这里，我们讨论了最近的发现，即酿酒酵母Elongator突变体的表型受遗传背景的调节。这种背景效应很大程度上是由于SSD1位点的等位基因变异所致，该位点编码一个参与基因表达的转录后调控的mRNA结合蛋白。在几种野生型实验室菌株中发现了一个无意义的ssd1等位基因，该等位基因的存在加剧了应力诱导的Elongator突变体表型。此外，其他表型，如组蛋白乙酰化和端粒基因沉默缺陷，也取决于突变的ssd1等位基因。因此，SSD1是延伸子缺陷型酵母细胞表型的遗传修饰子。在几种野生型实验室菌株中发现了一个无意义的ssd1等位基因，该等位基因的存在加剧了应力诱导的Elongator突变体表型。此外，其他表型，如组蛋白乙酰化和端粒基因沉默缺陷，也取决于突变的ssd1等位基因。因此，SSD1是延伸子缺陷型酵母细胞表型的遗传修饰子。在几种野生型实验室菌株中发现了一个无意义的ssd1等位基因，该等位基因的存在加剧了应力诱导的Elongator突变体表型。此外，其他表型，如组蛋白乙酰化和端粒基因沉默缺陷，也取决于突变的ssd1等位基因。因此，SSD1是延伸子缺陷型酵母细胞表型的遗传修饰子。