129922_GATCAG_2_1x_NMM_R1_001_edited_Reads_per_uniqueLocation.bw

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）结构可在富含鸟嘌呤的DNA或RNA中形成，并已被发现能调控细胞过程，包括复制、转录及翻译。关于G4细胞功能的众多研究集中于真核生物系统，而探究细菌G4的研究则少得多。利用化学遗传学方法，我们在<em>大肠杆菌（Escherichia coli）</em>中鉴定出在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（translation elongation factor Tu）的水平，或使用春日霉素（kasugamycin）、氯霉素（chloramphenicol）或壮观霉素（spectinomycin）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，会对G4稳定条件下的生长产生不利影响。蛋白质组学（proteomic）和转录组学（transcriptomic）分析表明，核糖体组装因子及其他参与翻译的蛋白质在G4稳定条件下的丰度降低。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。