The Transcription Regulator YgeK Affects Biofilm Formation and Environmental Stress Resistance in Avian Pathogenic Escherichia coli

SIMPLE SUMMARY: Avian pathogenic Escherichia coli (APEC) is the pathogen responsible for colibacillosis in poultry. Transcriptional regulator ygeK has been shown to decrease APEC’s flagellar formation ability, bacterial motility ability, serum sensitivity, and adhesion ability. However, we did not study the effects of ygeK on biofilm formation and environmental stress resistance in APEC. In this study, we investigated ygeK in APEC biofilm formation and bacterial resistance to different environmental stresses. We also analyzed the multi-level regulation of ygeK in APEC and investigated associations between differentially expressed proteins and key ygeK targets. This work provides a basis for further analysis of APEC pathogenesis mechanisms. ABSTRACT: Avian pathogenic Escherichia coli (APEC) is one of the most common pathogens in poultry and a potential gene source of human extraintestinal pathogenic E. coli (ExPEC), leading to serious economic losses in the poultry industry and public health concerns. Exploring the pathogenic mechanisms underpinning APEC and the identification of new targets for disease prevention and treatment are warranted. YgeK is a transcriptional regulator in APEC and is localized to the type III secretion system 2 of E. coli. In our previous work, the transcription factor ygeK significantly affected APEC flagella formation, bacterial motility, serum sensitivity, adhesion, and virulence. To further explore ygeK functions, we evaluated its influence on APEC biofilm formation and resistance to environmental stress. Our results showed that ygeK inactivation decreased biofilm formation and reduced bacterial resistance to environmental stresses, including acid and oxidative stress. In addition, the multi-level regulation of ygeK in APEC was analyzed using proteomics, and associations between differentially expressed proteins and the key targets of ygeK were investigated. Overall, we identified ygeK’s new function in APEC. These have led us to better understand the transcriptional regulatory ygeK and provide new clues about the pathogenicity of APEC.