Mironova L N, Zelenaia O A, Ter-Avanesian M D
Genetika. 1986 Feb;22(2):200-8.
An approach to the study of nuclear-mitochondrial interactions is reported. A number of spontaneous mutations compensating the respiratory deficiency in nuclear ribosomal suppressor mutants sup1 and sup2 were obtained and analysed. Among mutations analysed, mitochondrial as well as nuclear ones were found. Mitochondrial mutations neutralizing the expression of nuclear mutations were identified using the cytoduction test and their meiotic inheritance. The interaction of these mutations with sup1 and sup2 mutations resulting in restoration of respiratory competence was gene and allele nonspecific. Earlier we proposed that the respiratory deficiency of sup1 and sup2 mutants reflects the participation of sup1 and sup2 proteins not only in cytoplasmic, but also in mitochondrial translation. The interactions revealed open up the possibility of experimental examination of this hypothesis by means of identification of mitochondrial genes bearing compensating mutations.
报道了一种研究核-线粒体相互作用的方法。获得并分析了一些补偿核糖体抑制突变体sup1和sup2中呼吸缺陷的自发突变。在所分析的突变中,发现了线粒体突变以及核突变。利用细胞导入试验及其减数分裂遗传,鉴定了中和核突变表达的线粒体突变。这些突变与sup1和sup2突变相互作用导致呼吸能力恢复,具有基因和等位基因非特异性。我们之前提出,sup1和sup2突变体的呼吸缺陷不仅反映了sup1和sup2蛋白参与细胞质翻译,还参与线粒体翻译。所揭示的相互作用通过鉴定带有补偿性突变的线粒体基因,为实验检验这一假设开辟了可能性。