Data_Sheet_1_NrtR Regulates the Type III Secretion System Through cAMP/Vfr Pathway in Pseudomonas aeruginosa.PDF Yongxin Jin Mengjing Zhang Feng Zhu Qianqian Peng Yuding Weng Qiang Zhao Chang Liu Fang Bai Zhihui Cheng Shouguang Jin Weihui Wu 10.3389/fmicb.2019.00085.s001 https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_NrtR_Regulates_the_Type_III_Secretion_System_Through_cAMP_Vfr_Pathway_in_Pseudomonas_aeruginosa_PDF/7647686 <p>The type III secretion system (T3SS) plays an important role in the pathogenesis of Pseudomonas aeruginosa. Expression of the T3SS is controlled under a complicate regulatory network. In this study, we demonstrate that NrtR (PA4916) is involved in the T3SS expression and pathogenesis of P. aeruginosa in a mouse acute pneumonia model. Overexpression of the T3SS central activator ExsA or exogenous supplementation of cAMP restored the expression of T3SS in the ΔnrtR mutant, suggesting that NrtR might regulate T3SS through the cAMP-Vfr signaling pathway. Further experiments demonstrated that the decrease of cAMP content is not due to the expression change of adenylate cyclases or phosphodiesterase in the ΔnrtR mutant. As it has been shown that nadD2 is upregulated in the ΔnrtR mutant, we overexpressed nadD2 in wild type PAK, which reduced the intracellular cAMP level and the expression of the T3SS genes. Meanwhile, deletion of nadD2 in the ΔnrtR mutant restored the expression and secretion of the T3SS. Co-immunoprecipitation assay revealed an interaction between NadD2 and the catalytic domain of the adenylate cyclase CyaB. Further in vitro assay indicated that NadD2 repressed the enzymatic activity of CyaB. Therefore, we have identified a novel regulatory mechanism of T3SS in P. aeruginosa.</p> 2019-01-30 04:07:50 Pseudomonas aeruginosa NrtR cAMP CyaB type III secretion system