摘要
The flagella master regulatory gene flhDC of Yersinia pseudotuberculosis serotype III (YPIII) was mutated by deleting the middle region; replaced by a tetracycline resistant gene,; the subsequent mutant strain named YPIIIΔflhDC was obtained. Swimming assay showed that the swimming motility of the mutant strain was completely abolished. The promoter region of the flagella second-class regulatory gene fliA was fused with the lux box,; was conjugated with the mutant; the parent strains respectively for the first cross. LUCY assay result demonstrated that flhDC regulated the expression of fliA in YPIII as reported in E. coli. Biofilm formation of the mutant strain on abiotic; biotic surfaces was observed; quantified. The results showed that mutation of flhDC decreased biofilm formation on both abiotic; biotic surfaces,; abated the infection on Caenorhabdtis elegans. Our results suggest that mutation of the flagella master regulatory gene flhDC not only abolished the swimming motility, but also affected biofilm formation of YPIII on different surfaces. The new function of flhDC identified in this study provides a novel viewpoint for the control of bacterial biofilm formation.
The flagella master regulatory gene flhDC of Yersinia pseudotuberculosis serotype III (YPIII) was mu- tated by deleting the middle region and replaced by a tetracycline resistant gene, and the subsequent mutant strain named YPIII?flhDC was obtained. Swimming assay showed that the swimming motility of the mutant strain was completely abolished. The promoter region of the flagella second-class regula- tory gene fliA was fused with the lux box, and was conjugated with the mutant and the parent strains respectively for the first cross. LUCY assay result demonstrated that flhDC regulated the expression of fliA in YPIII as reported in E. coli. Biofilm formation of the mutant strain on abiotic and biotic surfaces was observed and quantified. The results showed that mutation of flhDC decreased biofilm formation on both abiotic and biotic surfaces, and abated the infection on Caenorhabdtis elegans. Our results suggest that mutation of the flagella master regulatory gene flhDC not only abolished the swimming motility, but also affected biofilm formation of YPIII on different surfaces. The new function of flhDC identified in this study provides a novel viewpoint for the control of bacterial biofilm formation.
作者
WANG Yao1, DING LiSha1,2, HU YangBo1,2, ZHANG Yong1,2, YANG BaoYu1 & CHEN ShiYun1 1 Wuhan Institute of Virology, Chinese Academy of Sciences, Wuhan 430071, China
2 Graduate University of Chinese Academy of Sciences, Beijing 100049, China
基金
Supported by the National Natural Science Foundation of China (Grant No. 30570020)
