Abstract
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.
Highlights
The bubonic plague causing bacillus, Yersinia pestis can be efficiently transmitted to a mammalian host through the formation of a robust biofilm in the foregut proventriculus of its flea vector
To understand which Y. pestis genes were essential for flea gut colonization and adaptation to produce a biofilm blockage-mediated transmissible infection we defined the unique transcriptome of Y. pestis in blocked fleas relative to LB in vitro growth conditions previously [1]
The competitive fitness defect exhibited by the rovM mutant during co-infection with the wild type suggests that lack of RovM leads to a deficiency at acquiring available nutrients in the flea gut
Summary
The bubonic plague causing bacillus, Yersinia pestis can be efficiently transmitted to a mammalian host through the formation of a robust biofilm in the foregut proventriculus of its flea vector. It was observed that the rovM gene encoding a LysR-type transcriptional regulator (LTTR), was highly upregulated in the flea gut only [1]. The LTTRs comprise a large family in prokaryotes and regulate diverse sets of genes involved in virulence, metabolism, motility and quorum sensing [2]. The Y. pestis RovM protein shares >65% overall identity with homologous LTTRs, LrhA/HexS/PecT/HexA, which regulate biofilm formation, synthesis of adhesins, extracellular polysaccharide, motility, exoenzymes, and exolipids, amongst other essential virulence factors in pathogenic Escherichia coli, Serratia spp., Erwinia spp. and entomopathogens, Photorhabdus temperata and Xenorhabdus nematophila [3,4,5,6,7,8]. Unlike the entomopathogens P. temperata and X. nematophila Y. pestis is avirulent to fleas [9]
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