Yuan Lingyue, Li Xuan, Du Ling, Su Kewen, Zhang Jiaxue, Liu Pin, He Qiang, Zhang Zhongshuang, Peng Dan, Shen Lifei, Qiu Jingfu, Li Yingli
School of Public Health and Management, Chongqing Medical University, Chongqing, China.
Hangzhou Hospital for the Prevention and Treatment of Occupational Disease, Hangzhou, China.
Front Cell Infect Microbiol. 2020 Jun 10;10:282. doi: 10.3389/fcimb.2020.00282. eCollection 2020.
The iron acquisition system is an essential virulence factor for human infection and is under tight regulatory control in a variety of pathogens. Ferric-uptake regulator (Fur) is one of Fe-responsive transcription factor that maintains iron homeostasis, and the regulator of capsule synthesis (Rcs) is known to regulate exopolysaccharide biosynthesis. We speculate the Rcs may involve in iron-acquisition given the identified regulator box in the upstream of that participated in the biosynthesis of enterobactin. To study the coregulation by RcsAB and Fur of , we measured the β-galactosidase activity and relative mRNA expression of in WT and mutant strains. The RcsAB- and Fur-protected regions were identified by an electrophoretic mobility shift assay (EMSA) and a DNase I footprinting assay. A regulatory cascade was identified with which Fur repressed expression and reduced RcsAB and expression. Our study demonstrated that was coregulated by two different transcriptional regulators, namely, RcsAB and Fur, in response to iron availability in .
铁摄取系统是人类感染的一种重要毒力因子，并且在多种病原体中受到严格的调控。铁摄取调节蛋白（Fur）是维持铁稳态的铁响应转录因子之一，而已知荚膜合成调节蛋白（Rcs）可调节胞外多糖的生物合成。鉴于在参与肠杆菌素生物合成的基因上游已鉴定出调节框，我们推测Rcs可能参与铁摄取。为了研究RcsAB和Fur对该基因的共同调控，我们测量了野生型和突变株中该基因的β-半乳糖苷酶活性和相对mRNA表达。通过电泳迁移率变动分析（EMSA）和DNase I足迹分析鉴定了RcsAB和Fur的保护区域。确定了一个调控级联，其中Fur抑制该基因的表达并降低RcsAB和该基因的表达。我们的研究表明，该基因受两种不同的转录调节因子RcsAB和Fur共同调控，以响应该菌中铁的可利用性。
