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G-quadruplex (G4) structures can form in guanine-rich DNA or RNA and have been found to modulate cellular processes, including replication, transcription, and translation. Many studies on the cellular roles of G4s have focused on eukaryotic systems, with far fewer probing bacterial G4s. Using a chemical-genetic approach, we identified genes in <em>Escherichia coli</em> that are important for growth in G4-stabilizing conditions. Reducing levels of translation elongation factor Tu or slowing translation initiation or elongation with kasugamycin, chloramphenicol, or spectinomycin suppress the effects of G4-stabilizing compounds. In contrast, reducing the expression of specific translation termination or ribosome recycling proteins is detrimental to growth in G4- stabilizing conditions. Proteomic and transcriptomic analyses demonstrate that ribosome assembly factors and other proteins involved in translation are less abundant in G4-stabilizing conditions. Our results support a model in which reducing the rate of translation by altering translation initiation/elongation, or ribosome assembly can compensate for G4-related stress in E. coli.

G-四链体（G-quadruplex，简称G4）结构可在富含鸟嘌呤的DNA或RNA中形成，且已被发现能调控多种细胞过程，包括复制、转录和翻译。关于G4细胞功能的研究多聚焦于真核生物系统，探究细菌G4的研究则少得多。我们采用化学遗传学方法，在<em>Escherichia coli</em>（大肠杆菌）中鉴定出了在G4稳定条件下对生长至关重要的基因。降低翻译延伸因子Tu的水平，或使用春日霉素、氯霉素或壮观霉素减缓翻译起始或延伸过程，均可抑制G4稳定化合物的效应。相反，降低特定翻译终止蛋白或核糖体回收蛋白的表达，在G4稳定条件下对生长有害。蛋白质组学和转录组学分析表明，核糖体组装因子及其他参与翻译过程的蛋白质在G4稳定条件下丰度降低。我们的结果支持一种模型：通过改变翻译起始/延伸过程或核糖体组装来降低翻译速率，可补偿大肠杆菌中与G4相关的应激。