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Abstract：
A yeast deletion mutation in the nuclear-encoded gene, AFO1, which codes for a mitochondrial ribosomal protein, led to slow growth on glucose, the inability to grow on glycerol or ethanol, and loss of mitochondrial DNA and respiration. We noticed that afo1- yeast readily obtains secondary mutations that suppress aspects of this phenotype, including its growth defect. We characterized and identified a dominant missense suppressor mutation in the ATP3 gene. Comparing isogenic slowly growing rho-zero and rapidly growing suppressed afo1- strains under carefully controlled fermentation conditions showed that energy charge was not significantly different between strains and was not causal for the observed growth properties. Surprisingly, in a wild-type background, the dominant suppressor allele of ATP3 still allowed respiratory growth but increased the petite frequency. Similarly, a slow-growing respiratory deficient afo1- strain displayed an about twofold increase in spontaneous frequency of point mutations (comparable to the rho-zero strain) while the suppressed strain showed mutation frequency comparable to the respiratory-competent WT strain. We conclude, that phenotypes that result from afo1- are mostly explained by rapidly emerging mutations that compensate for the slow growth that typically follows respiratory deficiency.
摘要：
核编码基因中的酵母缺失突变，AFO1编码一种线粒体核糖体蛋白,导致葡萄糖生长缓慢，无法在甘油或乙醇上生长，线粒体DNA和呼吸的丢失。我们注意到，afo1-酵母很容易获得抑制这种表型方面的次级突变，包括其生长缺陷。我们表征并鉴定了ATP3基因中的显性错义抑制突变。在精心控制的发酵条件下，比较等基因缓慢生长的rho-零和快速增长的受抑制的afo1-菌株表明，菌株之间的能量电荷没有显着差异，并且不是观察到的生长特性的原因。令人惊讶的是,在野生型背景下，ATP3的显性抑制等位基因仍然允许呼吸生长,但增加了小频率.同样，生长缓慢的呼吸缺陷型afo1-菌株显示点突变的自发频率增加了约两倍(与rho-zero菌株相当),而受抑制的菌株显示与有呼吸能力的WT菌株相当的突变频率.我们得出结论，由afo1-引起的表型主要由快速出现的突变解释，这些突变补偿了通常在呼吸缺陷之后的缓慢生长。
