Cells adjust to nutrient deprivation by reversible translational shutdown. This is accompanied by maintaining inactive ribosomes in a hibernation state, in which they are bound by proteins with inhibitory and protective functions. In eukaryotes, such a function was attributed to suppressor of target of Myb protein 1 (Stm1; SERPINE1 mRNA-binding protein 1 [SERBP1] in mammals), and recently, late-annotated short open reading frame 2 (Lso2; coiled-coil domain containing short open reading frame 124 [CCDC124] in mammals) was found to be involved in translational recovery after starvation from stationary phase. Here, we present cryo-electron microscopy (cryo-EM) structures of translationally inactive yeast and human ribosomes. We found Lso2/CCDC124 accumulating on idle ribosomes in the nonrotated state, in contrast to Stm1/SERBP1-bound ribosomes, which display a rotated state. Lso2/CCDC124 bridges the decoding sites of the small with the GTPase activating center (GAC) of the large subunit. This position allows accommodation of the duplication of multilocus region 34 protein (Dom34)-dependent ribosome recycling system, which splits Lso2-containing, but not Stm1-containing, ribosomes. We propose a model in which Lso2 facilitates rapid translation reactivation by stabilizing the recycling-competent state of inactive ribosomes.

细胞通过可逆的翻译关闭来适应营养的缺乏。这伴随着使无活性核糖体保持在冬眠状态，其中它们被具有抑制和保护功能的蛋白质结合。在真核生物中，这种功能归因于Myb蛋白1（Stm1； SERPINE1 mRNA结合蛋白1 [SERBP1]，在哺乳动物中）的靶标的抑制子，最近归功于后期注释的短开放阅读框2（Lso2；卷曲螺旋结构域）。含有短开放阅读框124 [在哺乳动物中的CCDC124]被发现与从固定相饥饿后的翻译恢复有关。在这里，我们介绍了平移非活性酵母和人类核糖体的低温电子显微镜（cryo-EM）结构。与结合Stm1 / SERBP1的核糖体相反，我们发现Lso2 / CCDC124在非旋转状态的闲置核糖体上积累，显示旋转状态。Lso2 / CCDC124将小分子的解码位点与大亚基的GTPase激活中心（GAC）桥接在一起。该位置允许适应多位点区域34蛋白（Dom34）依赖的核糖体回收系统的复制，该系统可分离含Lso2的核糖体，而不分离含Stm1的核糖体。我们提出了一种模型，其中Lso2通过稳定无活性核糖体的可回收状态来促进快速翻译重新激活。