A LysR-Type Transcriptional Regulator, RovM, Senses Nutritional Cues Suggesting that It Is Involved in Metabolic Adaptation of Yersinia pestis to the Flea Gut.
Yersinia pestis has evolved as a clonal variant of Yersinia pseudotuberculosis to cause flea-borne biofilm-mediated transmission of the bubonic plague. The LysR-type transcriptional regulator, RovM, is highly induced only during Y. pestis infection of the flea host. RovM homologs in other pathogens regulate biofilm formation, nutrient sensing, and virulence; including in Y. pseudotuberculosis, where RovM represses the major virulence factor, RovA. Here the role that RovM plays during flea infection was investigated using a Y. pestis KIM6+ strain deleted of rovM, ΔrovM. The ΔrovM mutant strain was not affected in characteristic biofilm gut blockage, growth, or survival during single infection of fleas. Nonetheless, during a co-infection of fleas, the ΔrovM mutant exhibited a significant competitive fitness defect relative to the wild type strain. This competitive fitness defect was restored as a fitness advantage relative to the wild type in a ΔrovM mutant complemented in trans to over-express rovM. Consistent with this, Y. pestis strains, producing elevated transcriptional levels of rovM, displayed higher growth rates, and differential ability to form biofilm in response to specific nutrients in comparison to the wild type. In addition, we demonstrated that rovA was not repressed by RovM in fleas, but that elevated transcriptional levels of rovM in vitro correlated with repression of rovA under specific nutritional conditions. Collectively, these findings suggest that RovM likely senses specific nutrient cues in the flea gut environment, and accordingly directs metabolic adaptation to enhance flea gut colonization by Y. pestis.
Paul G. Allen School for Global Animal Health, Washington State University, Pullman, Washington, 99164, United States of America.
Viveka
V
Vadyvaloo
Paul G. Allen School for Global Animal Health, Washington State University, Pullman, Washington, 99164, United States of America.
Angela K
AK
Hinz
D000818:Animals; D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics*; D018441:Biofilms / Q000254:growth & development; D060085:Coinfection / Q000235:genetics; D058267:Flea Infestations / Q000235:genetics / Q000473:pathology; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D007303:Insect Vectors / Q000235:genetics / Q000472:pathogenicity; D010930:Plague / Q000235:genetics* / Q000473:pathology / Q000635:transmission; D005423:Siphonaptera / Q000235:genetics / Q000472:pathogenicity; D014157:Transcription Factors / Q000096:biosynthesis / Q000235:genetics*; D015010:Yersinia pestis / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity; D015011:Yersinia pseudotuberculosis / Q000235:genetics / Q000472:pathogenicity
D001426:Bacterial Proteins; C405626:RovA protein, Yersinia; C517503:RovM protein, Yersinia pseudotuberculosis; D014157:Transcription Factors