Inactivation of ssrB in the ydgT background resulted in complete loss of virulence during systemic infection , consistent with the finding that deletion of ydgT does not override the requirement of SsrB for transcriptional activation of the SPI-2 pathogenicity island .
Taken together , these lines of evidence suggest that the Fur repressor could interfere with binding of the SsrB activator to the ssrB promoter , leading to repression of ssrB transcription .