The invasion and colonization of host plants by the destructive pathogen Ralstonia solanacearum rely on its cell motility, which is controlled by multiple factors. Here, we report that the LysR-type transcriptional regulator CrgA (RS_RS16695) represses cell motility in R. solanacearum GMI1000. CrgA possesses common features of a LysR-type transcriptional regulator and contains an N-terminal helix-turn-helix motif as well as a C-terminal LysR substrate-binding domain. Deletion of crgA results in an enhanced swim ring and increased transcription of flhDC. In addition, the ΔcrgA mutant possesses more polar flagella than wild-type GMI1000 and exhibits higher expression of the flagellin gene fliC. Despite these alterations, the ΔcrgA mutant did not have a detectable growth defect in culture. Yeast one-hybrid and electrophoretic mobility shift assays revealed that CrgA interacts directly with the flhDC promoter. Expressing the β-glucuronidase (GUS) reporter under the control of the crgA promoter showed that crgA transcription is dependent on cell density. Soil-soaking inoculation with the crgA mutant caused wilt symptoms on tomato (Solanum lycopersicum L. cv. Hong yangli) plants earlier than inoculation with the wild-type GMI1000 but resulted in lower disease severity. We conclude that the R. solanacearum regulator CrgA represses flhDC expression and consequently affects the expression of fliC to modulate cell motility, thereby conditioning disease development in host plants.

中文翻译：

---

LysR型转录调节剂CrgA负调控青枯雷尔氏菌GMI1000中的鞭毛主调节剂flhDC。

破坏性病原体青枯雷尔氏菌对宿主植物的入侵和定植依赖于其细胞运动性，其受多种因素控制。在这里，我们报告说，LysR型转录调节子CrgA（RS_RS16695）抑制青枯菌GMI1000中的细胞运动。CrgA具有LysR型转录调节子的共同特征，并包含N末端螺旋-转-螺旋基序以及C末端LysR底物结合域。删除crgA导致增强游泳环和增加flhDC的转录。此外，ΔcrgA突变体比野生型GMI1000具有更多的极性鞭毛，并且鞭毛蛋白基因fliC的表达更高。尽管有这些变化，但ΔcrgA突变体在培养中没有可检测到的生长缺陷。酵母一杂交和电泳迁移率迁移分析表明，CrgA与flhDC启动子直接相互作用。在crgA启动子的控制下表达β-葡萄糖醛酸酶（GUS）报告基因表明crgA转录取决于细胞密度。与野生型GMI1000相比，使用crgA突变体对土壤进行浸泡接种会比番茄（Solanum lycopersicum L. cv。Hong yangli）更早出现番茄症状。我们得出结论，青枯菌调节剂CrgA抑制flhDC。表达并因此影响fliC的表达以调节细胞运动，从而调节宿主植物中的疾病发展。