Genetic and Proteomic Analyses of a Xanthomonas campestris pv.campestris purC Mutant Deficient in Purine Biosynthesis and Virulence  

作　　者：Zhihui Yuan Li Wang Shutao Sun Yao Wu Wei Qian 

机构地区：[1]State Key Laboratory of Plant Genomics,Institute of Microbiology,Chinese Academy of Sciences [2]University of Chinese Academy of Sciences [3]Center of Core Facility,Institute of Microbiology,Chinese Academy of Sciences

出　　处：《Journal of Genetics and Genomics》2013年第9期473-487,共15页遗传学报（英文版）

基　　金：supported by the grants from the National Basic Research Program of the Ministry of Science and Technology of China(No.2011CB100700);the National Science Foundation of China(Nos.31100065 and 31070081);the Basic Research of Frontiers of the Chinese Academy of Sciences(No.KSCX2-EW-J-6)

摘　　要：Bacterial proliferation in hosts requires activation of a number of housekeeping pathways, including purine de novo biosynthesis. Although inactivation of purine biosynthesis genes can attenuate virulence, it is unclear which biochemical or virulence factors are associated with the purine biosynthesis pathway in vivo. We report that inactivation of purC, a gene encoding phosphoribosylaminoimidazole-succinocarboxamide synthase, caused complete loss of virulence in Xanthomonas campestris pv. cam- pestris, the causal agent of black rot disease of cruciferous plants. The purC mutant was a purine auxotroph; it could not grow on minimal medium, whereas addition of purine derivatives, such as hypoxanthine or adenine plus guanine, restored growth of the mutant. The purC mutation also significantly enhanced the production of an unknown purine synthesis associated pigment and extracellular polysaccharides by the bacterium. In addition, comparative proteomic analyses of bacteria grown on rich and minimal media revealed that the purC mutation affected the expression levels of diverse proteins involved in purine and pyrimidine synthesis, carbon and energy metabolisms, iron uptake, proteolysis, protein secretion, and signal transduction. These results provided clues to understanding the contributions of purine synthesis to bacterial virulence and interactions with host immune systems.Bacterial proliferation in hosts requires activation of a number of housekeeping pathways, including purine de novo biosynthesis. Although inactivation of purine biosynthesis genes can attenuate virulence, it is unclear which biochemical or virulence factors are associated with the purine biosynthesis pathway in vivo. We report that inactivation of purC, a gene encoding phosphoribosylaminoimidazole-succinocarboxamide synthase, caused complete loss of virulence in Xanthomonas campestris pv. cam- pestris, the causal agent of black rot disease of cruciferous plants. The purC mutant was a purine auxotroph; it could not grow on minimal medium, whereas addition of purine derivatives, such as hypoxanthine or adenine plus guanine, restored growth of the mutant. The purC mutation also significantly enhanced the production of an unknown purine synthesis associated pigment and extracellular polysaccharides by the bacterium. In addition, comparative proteomic analyses of bacteria grown on rich and minimal media revealed that the purC mutation affected the expression levels of diverse proteins involved in purine and pyrimidine synthesis, carbon and energy metabolisms, iron uptake, proteolysis, protein secretion, and signal transduction. These results provided clues to understanding the contributions of purine synthesis to bacterial virulence and interactions with host immune systems.

关 键 词：Purine biosynthesis VIRULENCE Xanthomonas campestris pv. campestris PROTEOMICS 

分 类 号：S435.654[农业科学—农业昆虫与害虫防治]