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.

酵母细胞核编码基因AFO1 （编码线粒体核糖体蛋白）中的缺失突变导致酵母在葡萄糖下生长缓慢，无法在甘油或乙醇下生长，以及线粒体 DNA 和呼吸的丧失。我们注意到afo1 ^-酵母很容易获得二次突变，抑制该表型的各个方面，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。在仔细控制的发酵条件下比较等基因缓慢生长的 rho-0 菌株和快速生长的受抑制的afo1^菌株表明，菌株之间的能量负荷没有显着差异，并且与观察到的生长特性无关。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，但增加了娇小的频率。类似地，生长缓慢的呼吸缺陷afo1-菌株显示点突变的自发频率增加约两倍（与rho-零菌株^相比），而抑制菌株显示出与具有呼吸能力的WT菌株相当的突变频率。我们得出的结论是， afo1^产生的表型主要是通过快速出现的突变来解释的，这些突变弥补了呼吸缺陷后通常出现的缓慢生长。