Takallou Sarah, Hajikarimlou Maryam, Al-Gafari Mustafa, Wang Jiashu, Kazmirchuk Thomas David Daniel, Said Kamaledin B, Samanfar Bahram, Golshani Ashkan
Ottawa Institute of Systems Biology, University of Ottawa, Ottawa, ON K1N 6N5, Canada.
Department of Biology, Carleton University, Ottawa, ON K1S 5B6, Canada.
Biology (Basel). 2024 Feb 22;13(3):138. doi: 10.3390/biology13030138.
Maintaining translation fidelity is a critical step within the process of gene expression. It requires the involvement of numerous regulatory elements to ensure the synthesis of functional proteins. The efficient termination of protein synthesis can play a crucial role in preserving this fidelity. Here, we report on investigating a protein of unknown function, (also known as ), for its activity in the process of translation. We observed a significant increase in the bypass of premature stop codons upon the deletion of . Interestingly, the genomic arrangement of this ORF suggests a compatible mode of expression reliant on translational readthrough, incorporating the neighboring open reading frame. We also showed that the deletion of results in an increase in the rate of translation. Based on our results, we propose that may play a role in translation fidelity, impacting the overall quantity and quality of translation. Our genetic interaction analysis supports our hypothesis, associating the role of to the regulation of protein synthesis.
维持翻译保真度是基因表达过程中的关键步骤。这需要众多调控元件的参与以确保功能性蛋白质的合成。蛋白质合成的有效终止在维持这种保真度方面可发挥关键作用。在此，我们报告对一种功能未知的蛋白质（也称为 ）在翻译过程中的活性进行研究。我们观察到缺失 后，提前终止密码子的通读显著增加。有趣的是，该开放阅读框（ORF）的基因组排列表明其存在一种依赖翻译通读的兼容表达模式，其中纳入了相邻的开放阅读框。我们还表明缺失 会导致翻译速率增加。基于我们的结果，我们提出 可能在翻译保真度中发挥作用，影响翻译的整体数量和质量。我们的遗传相互作用分析支持了我们的假设，将 的作用与蛋白质合成的调控联系起来。
