129921_ACTTGA_1_2x_NMM_R1_001_edited_Reads_per_uniqueLocation.wig

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，G4）可在富含鸟嘌呤的DNA或RNA中形成，且已被证实可调控包括复制、转录及翻译在内的多种细胞过程。既往针对G4细胞功能的诸多研究多聚焦于真核生物系统，对细菌G4的探索则相对匮乏。本研究采用化学遗传学方法，在大肠杆菌（Escherichia coli）中筛选出在G4稳定化条件下对菌体生长至关重要的基因。通过降低翻译延伸因子Tu（translation elongation factor Tu）的表达水平，或使用春日霉素（kasugamycin）、氯霉素（chloramphenicol）、壮观霉素（spectinomycin）减缓翻译起始或延伸过程，可抑制G4稳定化化合物的作用效果。与之相反，降低特定翻译终止蛋白或核糖体回收蛋白的表达，则会对G4稳定化条件下的菌体生长产生不利影响。蛋白质组学与转录组学分析结果显示，在G4稳定化条件下，核糖体组装因子及其他参与翻译过程的蛋白丰度均有所降低。本研究结果支持如下模型：通过改变翻译起始/延伸过程或核糖体组装以降低翻译速率，可补偿大肠杆菌中由G4介导的应激压力。