Rinaldi T, Francisci S, Zennaro E, Frontali L, Bolotin-Fukuhara M
Laboratoire de Génétique Moléculaire, Université Paris-Sud, Orsay, France.
Curr Genet. 1994 May;25(5):451-5. doi: 10.1007/BF00351785.
We used a genetic approach to study the nuclear factors involved in the biogenesis of mitochondrial tRNAs. A point mutation in the mitochondrial tRNA(Asp) gene of Saccharomyces cerevisiae had previously been shown to result in a temperature-sensitive respiratory-deficient phenotype as a result of the absence of 3' end-processing of the tRNA(Asp). Analysis of mitochondrial revertants has shown that all revertants sequenced have a G-A compensatory change at position 53, which restores the hydrogen-bond with the mutated nucleotide. We then searched for nuclear suppressors to identify the nuclear gene(s) involved in mitochondrial tRNA 3' end-processing. One such suppressor mutation was further characterized: it restores tRNA(Asp) maturation and growth at 36 degrees C on glycerol medium in heterozygous diploids, but leads to a defective growth phenotype in haploids.
我们采用遗传学方法来研究参与线粒体tRNA生物合成的核因子。先前已表明，酿酒酵母线粒体tRNA（Asp）基因中的一个点突变会导致温度敏感型呼吸缺陷表型，这是由于tRNA（Asp）缺乏3'末端加工所致。对线粒体回复突变体的分析表明，所有测序的回复突变体在第53位都有一个G-A补偿性变化，该变化恢复了与突变核苷酸的氢键。然后，我们寻找核抑制因子以鉴定参与线粒体tRNA 3'末端加工的核基因。对其中一个这样的抑制突变进行了进一步表征：它能恢复杂合二倍体中tRNA（Asp）的成熟以及在36摄氏度甘油培养基上的生长，但会导致单倍体出现生长缺陷表型。
