Abstract:[Background] Xanthomonas campestris pv. campestris (Xcc) is the pathogen of black rot in cruciferous plants, causing immense economic losses worldwide. Therefore, it is urgent to study the pathogenic mechanism of this pathogen and develop novel methods to control this disease. The bacterial fatty acid synthesis system provides not only substrates for cell membrane synthesis but also the intermediates to be used as precursors for the synthesis of bioactive molecules. With important functions, the fatty acid synthesis system is a promising target for the screening of antibacterial agents. [Objective] To investigate the effects of Xcc fabZ on the diffusible signal factor (DSF) family signals production, pathogenicity, extracellular enzymes, extracellular polysaccharides, and motility of Xcc. [Methods] The yields of DSF family signals produced by different strains were estimated by the bioassay method with the DSF reporter strain. The replacement mutants were established from the DSF family signals high yield strain based on homologous recombination. Then, the yields of DSF family signals were determined by high performance liquid chromatography (HPLC). The pathogenicity of different strains to the host plant Brassica oleracea L. was examined by the leaf-clipping method, and the production of exopolysaccharides (EPS), extracellular enzymes, and motility were compared among different strains. [Results] The DSF family signals produced by the Escherichia coli fabZ replacement mutant (Xcc ΔfabZ/pSRK-EcfabZ) decreased sharply. Moreover, the mutant presented attenuated pathogenicity to the host plant, slow growth in the plant extract, reduced extracellular enzyme production, and weakened motility. The production of DSF family signals by the Xcc fabZ replacement mutant was restored to the level of the wild-type strain, and excessive production of EPS enhanced the pathogenicity and restored the extracellular enzymes and motility. [Conclusion] FabZ affects the production of DSF family signals and extracellular enzymes, pathogenicity, and motility of Xcc.