RtxA1 Toxin Expression Upon Contact With Host Cells Is RpoS-Dependent.

The expression of virulence genes in bacteria is known to be regulated by various environmental and host factors. , an estuarine bacterium, experiences a dramatic environmental change during its infection process. We reported that RtxA1 toxin caused acute cell death only when close contact to host cells was allowed. A sigma factor RpoS is a very important regulator for the maximal survival of pathogens under stress conditions. Here, we studied the role of RpoS in cytotoxicity and mouse lethality. The growth of mutant strain was comparable to that of wild-type in heart infusion (HI) media and DMEM with HeLa cell lysate. An mutation resulted in decreased cytotoxicity, which was restored by complementation. Interestingly, host contact increased the expression and secretion of RtxA1 toxin, which was decreased and delayed by the mutation. Transcription of the cytotoxic gene and its transporter was significantly increased after host factor contact, whereas the activity was decreased by the mutation. In contrast, the mutation showed no effect on the transcriptional activity of a cytolytic heamolysin gene (). Additionally, the LD of the mutant was 15-fold higher than that of the wild-type in specific pathogen-free CD-1 female mice. Taken together, these results show that RpoS regulates the expression of RtxA1 toxin and its transporter upon host contact.