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Negative Regulation of RpoS-mediated STM1703 in Biofilm Formation of Salmonella Pullorum
Zheng Feng1,2,3,4, Muhanad El Hag1,2,3,4, Nan Wang1,2,3,4, Tao Qin1,2,3,4, Sujuan Chen1,2,3,4 and Daxin Peng1,2,3,4*

1College of Veterinary Medicine, Yangzhou University, Yangzhou 225009, Jiangsu, PR China
2Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou 225009, Jiangsu, PR China
3Jiangsu Research Centre of Engineering and Technology for Prevention and Control of Poultry Disease, Yangzhou 225009, Jiangsu, PR China
4Joint Laboratory Safety of International Cooperation of Agriculture and Agricultural-Products, Ministry of Education, Yangzhou University, PR China
*Corresponding author:


Both alternative sigma factor RpoS and ubiquitous secondary messenger c-di-GMP participate in the biofilm forming of Salmonella Pullorum; however, the relationship between RpoS and c-di-GMP-regulated genes during biofilm forming remains unclear. In this study, nine genes related with c-di-GMP regulation were found to be differentially expressed (P<0.01) by RNA-seq analysis when compared with S. Pullorum strain S9 and its rpoS deletion strain S9S. Specifically, the rpoS deletion strain S9S had higher transcription level of gene STM1703 and lower c-di-GMP concentration and biofilm-forming ability than S9 (P<0.01). The STM1703 gene deletion in strains S9 and S9S significantly enhanced the c-di-GMP concentration and the biofilm-forming ability (P<0.01). qRT–PCR analysis showed that rpoS deletion or P193L substitution in RpoS increased the transcription level of the STM1703 gene by decreasing the transcription levels of the csrA and STM1344 genes (P<0.01). Overall, RpoS-mediated STM1703 negatively regulates the biofilm formation of S. Pullorum by degrading c-di-GMP.

To Cite This Article: Feng Z, Hag ME, Wang N, Qin T, Chen S and Peng D, 2022. Negative regulation of RpoS-mediated STM1703 in biofilm formation of Salmonella pullorum. Pak Vet J.


ISSN 0253-8318 (Print)
ISSN 2074-7764 (Online)