The Gram‐negative soil‐borne bacterium Ralstonia solanacearum first infects roots of host plants and then invades xylem vessels. In xylem vessels, the bacteria grow vigorously and produce exopolysaccharides (EPSs) to cause a wilt symptom on host plants. The EPSs are thus the main virulence factors of R. solanacearum. The strain OE1‐1 of R. solanacearum produces methyl 3‐hydroxymyristate as a quorum‐sensing (QS) signal, and senses this QS signal, activating QS. The QS‐activated LysR‐type transcriptional regulator PhcA induces the production of virulence‐related metabolites including ralfuranone and the major EPS, EPS I. To elucidate the function of EPS I, the transcriptomes of R. solanacearum strains were analysed using RNA sequencing technology. The expression of 97.2% of the positively QS‐regulated genes was down‐regulated in the epsB‐deleted mutant ΔepsB, which lost its EPS I productivity. Furthermore, expression of 98.0% of the negatively QS‐regulated genes was up‐regulated in ΔepsB. The deficiency to produce EPS I led to a significantly suppressed ralfuranone productivity and significantly enhanced swimming motility, which are suppressed by QS, but did not affect the expression levels of phcA and phcB, which encode a methyltransferase required for methyl 3‐hydroxymyristate production. Overall, QS‐dependently produced EPS I may be associated with the feedback loop of QS.

中文翻译：

---

主要胞外多糖EPS I与青枯雷尔氏菌菌株OE1-1的群体感应中的反馈环相关。

革兰氏阴性土传细菌Ralstonia solanacearum首先感染宿主植物的根，然后侵入木质部容器。在木质部的容器中，细菌旺盛生长并产生胞外多糖（EPS），导致宿主植物出现枯萎症状。因此，EPS是青枯菌的主要毒力因子。青枯菌的OE1-1菌株产生3-羟基肉豆蔻酸甲酯作为群体感应（QS）信号，并感测此QS信号，从而激活QS。经QS激活的LysR型转录调节剂PhcA诱导了与毒性相关的代谢产物的产生，包括雷呋喃酮和主要的EPS，EPSI。为阐明EPS I的功能，即茄形假单胞菌的转录组。使用RNA测序技术分析菌株。97.2％的正QS调控基因的表达在epsB缺失的突变体ΔepsB中被下调，从而失去了其EPS I生产率。此外，ΔepsB中98.0％的QS负调控基因的表达上调。产生EPS I的缺乏导致QF抑制了雷呋喃酮的生产能力显着降低和游泳运动的增强，但并未影响phcA和phcB的表达水平，而phcA和phcB的表达水平是生产3-羟基肉豆蔻酸甲酯所需的甲基转移酶。总的来说，由QS产生的EPS I可能与QS的反馈回路有关。