Department of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195-6540, USA; Mitochondria and Metabolism Center, University of Washington, 850 Republican Street, Seattle, WA 98105, USA.
Department of Genome Sciences, University of Washington, 3720 15th Ave NE, Seattle, WA 98105, USA.
Curr Biol. 2021 Jan 11;31(1):128-137.e5. doi: 10.1016/j.cub.2020.10.001. Epub 2020 Nov 5.
The translation machinery is composed of a myriad of proteins and RNAs whose levels must be coordinated to efficiently produce proteins without wasting energy or substrate. However, protein synthesis is clearly not always perfectly tuned to its environment, as disruption of translation machinery components can lengthen lifespan and stress survival. While much has been learned from bacteria and yeast about translational regulation, much less is known in metazoans. In a screen for mutations protecting C. elegans from hypoxic stress, we isolated multiple genes impacting protein synthesis: a ribosomal RNA helicase gene, tRNA biosynthesis genes, and a gene controlling amino acid availability. To define better the mechanisms by which these genes impact protein synthesis, we performed a second screen for suppressors of the conditional developmental arrest phenotype of the RNA helicase mutant and identified genes involved in ribosome biogenesis. Surprisingly, these suppressor mutations restored normal hypoxic sensitivity and protein synthesis to the tRNA biogenesis mutants, but not to the mutant reducing amino acid uptake. Proteomic analysis demonstrated that reduced tRNA biosynthetic activity produces a selective homeostatic reduction in ribosomal subunits, thereby offering a mechanism for the suppression results. Our study uncovers an unrecognized higher-order-translation regulatory mechanism in a metazoan whereby ribosome biogenesis genes communicate with genes controlling tRNA abundance matching the global rate of protein synthesis with available resources.
翻译机制由无数的蛋白质和 RNA 组成,其水平必须协调,以有效地产生蛋白质,而不浪费能量或底物。然而,蛋白质合成显然并不总是完全适应其环境,因为翻译机制成分的破坏可以延长寿命和应激生存。虽然已经从细菌和酵母中了解到了很多关于翻译调控的知识,但在后生动物中却知之甚少。在筛选保护秀丽隐杆线虫免受缺氧应激的突变体时,我们分离出了多个影响蛋白质合成的基因:一个核糖体 RNA 解旋酶基因、tRNA 生物合成基因和一个控制氨基酸可用性的基因。为了更好地定义这些基因影响蛋白质合成的机制,我们进行了第二次筛选,以寻找 RNA 解旋酶突变体的条件发育阻滞表型的抑制子,并鉴定了参与核糖体生物发生的基因。令人惊讶的是,这些抑制突变恢复了 tRNA 生物合成突变体的正常缺氧敏感性和蛋白质合成,但不能恢复减少氨基酸摄取的突变体。蛋白质组学分析表明,减少 tRNA 生物合成活性会导致核糖体亚基的选择性稳态减少,从而为抑制结果提供了一种机制。我们的研究揭示了后生动物中一种未被认识的更高层次的翻译调控机制,即核糖体生物发生基因与控制 tRNA 丰度的基因进行通讯,使全球蛋白质合成率与可用资源相匹配。