Regulatory crosstalk between motility and interbacterial communication in Salmonella Typhimurium

Abstract

FliA is a broadly conserved {sigma} factor that directs transcription of genes involved in flagellar motility. We previously identified FliA-transcribed genes in Escherichia coli and Salmonella enterica serovar Typhimurium, and we showed that E. coli FliA transcribes many unstable, non-coding RNAs from intragenic promoters. Here, we show that FliA in S. Typhimurium also directs transcription of large numbers of unstable, non-coding RNAs from intragenic promoters, and we identify two previously unreported FliA-transcribed protein-coding genes. One of these genes, sdiA, encodes a transcription factor that responds to quorum sensing signals produced by other bacteria. We show that FliA-dependent transcription of sdiA is required for SdiA activity, highlighting a regulatory link between flagellar motility and intercellular communication. IMPORTANCEInitiation of bacterial transcription requires association of a {sigma} factor with the core RNA polymerase to facilitate sequence-specific recognition of promoter elements. FliA is a widely conserved {sigma} factor that directs transcription of genes involved in flagellar motility. We previously showed that Escherichia coli FliA transcribes many unstable, non-coding RNAs from promoters within genes. Here, we demonstrate the same phenomenon in Salmonella Typhimurium. We also show that S. Typhimurium FliA directs transcription of the sdiA gene, which encodes a transcription factor that responds to quorum sensing signals produced by other bacteria. FliA-dependent transcription of sdiA is required for transcriptional control of SdiA target genes, highlighting a regulatory link between flagellar motility and intercellular communication.