Experimental evidence for negative selection in the evolution of a Yersinia pestis pseudogene

Abstract

Yersinia pestis, the agent of bubonic plague, evolved from the enteric pathogen Yersinia pseudotuberculosis within the past 20,000 years. Because ancestor and descendant both exist, it is possible to infer steps in molecular evolution by direct experimental approaches. The Y. pestis life cycle includes establishment of a biofilm within its vector, the flea. Although Y. pseudotuberculosis makes biofilms in other environments, it fails to do so in the insect. We show that rcsA, a negative regulator of biofilms that is functional in Y. pseudotuberculosis, is a pseudogene in Y. pestis. Replacement of the pseudogene with the functional Y. pseudotuberculosis rcsA allele strongly represses biofilm formation and essentially abolishes flea biofilms. The conversion of rcsA to a pseudogene during Y. pestis evolution, therefore, was a case of negative selection rather than neutral genetic drift.biofilm ͉ flea ͉ bubonic plague ͉ phosphorelay ͉ Caenorhabditis elegans

Adhesive Properties of YapV and Paralogous Autotransporter Proteins of Yersinia pestis

“…Comparative genomics has led to the consideration of Y. pestis zation, as biofilm formation in fleas benefits bacterial transmission (56,57). The pseudogenization or absence of yapX in full Y. pestis genomes confirms the pattern of reductive loss in this bacterium compared to Y. pseudotuberculosis.…”

Antimicrobial Pressure of Ciprofl oxacin and Gentamicin on Biofi lm Development by an Endoscope-Isolated Pseudomonas aeruginosa

“…Biofilm-forming bacteria growing on the agar plate can give a rugose colony morphology in which the cells are embedded in abundant biofilm exopolysaccharide, and the degrees of rugose colony morphology positively reflect the ability to synthesize the biofilm exopolysaccharide [9,25,26]. Dfur produced colonies with much more rugose morphology in relative to WT that was comparable to C-fur, while DhmsS made the smooth colonies (Fig.…”

Formation and regulation of Yersinia biofilms

“…The sensor kinases RcsC and RcsD transfer phosphate to RcsB; activated by the phosphorylation, the DNA-binding regulator RcsB regulates the transcription of some targets independently, whereas other targets require the accessory protein RcsA (Majdalani and Gottesman, 2005). The Rcs system negatively regulates Yersinia biofilm production in both nematode and flea models (Sun et al, 2008). The RcsAB consensus-like sequences are located within the promoter regions of both hmsHFRS and hmsT, indicating that they might serve as the direct targets of RcsAB.…”

“…Both RcsA and NghA are functional in Y. pseudotuberculosis, but their structural genes are inactivated in Y. pestis Sun et al, 2008). Expression of functional RcsA or NghA in Y. pestis strongly represses biofilm formation and essentially abolishes flea blockage .…”