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Simple Summary  Avian pathogenic  Escherichia coli  (APEC) is the responsible pathogen for colibacillosis in poultry. Transcriptional regulator YgeK was a transcriptional regulator locating at  E. coli  type three secretion system 2 (ETT2) in APEC. However, the role of YgeK in APEC has not been reported. In this study, we found that the inactivation of YgeK in APEC decreased the flagellar formation ability, bacterial motility ability, serum sensitivity, adhesion ability, and virulence. Results suggested that the transcriptional regulator YgeK plays a crucial role in APEC virulence.    Abstract  Avian pathogenic  Escherichia coli  (APEC) is the responsible pathogen for colibacillosis in poultry, and is a potential gene source for human extraintestinal pathogenic  Escherichia coli .  Escherichia coli  type III secretion system 2 (ETT2) is widely distributed in human and animal ExPEC isolates, and is crucial for the virulence of ExPEC. Transcriptional regulator YgeK, located in the ETT2 gene cluster, was identified as an important regulator of gene expression in enterohemorrhagic  E. coli  (EHEC). However, the role of YgeK in APEC has not been reported. In this study, we performed amino acid alignment analysis of YgeK among different  E. coli  strains and generated ygeK mutant strain AE81Δ ygeK  from clinical APEC strain AE81. Flagellar formation, bacterial motility, serum sensitivity, adhesion, and virulence were all significantly reduced following the inactivation of YgeK in APEC. Then, we performed transcriptome sequencing to analyze the functional pathways involved in the biological processes. Results suggested that ETT2 transcriptional regulator YgeK plays a crucial role in APEC virulence. These findings thus contribute to our understanding of the function of the ETT2 cluster, and clarify the pathogenic mechanism of APEC.

Transcription Regulator YgeK Affects the Virulence of Avian Pathogenic Escherichia coli