Abstract
The delta subunit of the RNA polymerase, RpoE, maintains the transcriptional specificity in Gram-positive bacteria. Lack of RpoE results in massive changes in the transcriptome of the human dental caries pathogen Streptococcus mutans. In this study, we analyzed traits of the ΔrpoE mutant which are important for biofilm formation and interaction with oral microorganisms and human cells and performed a global phenotypic analysis of its physiological functions. The ΔrpoE mutant showed higher self-aggregation compared to the wild type and coaggregated with other oral bacteria and Candida albicans. It formed a biofilm with a different matrix structure and an altered surface attachment. The amount of the cell surface antigens I/II SpaP and the glucosyltransferase GtfB was reduced. The ΔrpoE mutant displayed significantly stronger adhesion to human extracellular matrix components, especially to fibronectin, than the wild type. Its adhesion to human epithelial cells HEp-2 was reduced, probably due to the highly aggregated cell mass. The analysis of 1248 physiological traits using phenotype microarrays showed that the ΔrpoE mutant metabolized a wider spectrum of carbon sources than the wild type and had acquired resistance to antibiotics and inhibitory compounds with various modes of action. The reduced antigenicity, increased aggregation, adherence to fibronection, broader substrate spectrum and increased resistance to antibiotics of the ΔrpoE mutant reveal the physiological potential of S. mutans and show that some of its virulence related traits are increased.
Highlights
Streptococcus mutans is the main causative agent of human dental caries, which is one of the most prevailing infectious diseases in the world [1]
Increased self- and co-aggregation in the DrpoE mutant The S. mutans cells from the stationary growth phase were used for the self-aggregation analysis
Proteinase K treatment strongly reduced the self-aggregation of the DrpoE mutant, suggesting that surface proteins contribute to its selfaggregation
Summary
Streptococcus mutans is the main causative agent of human dental caries, which is one of the most prevailing infectious diseases in the world [1]. Since S. mutans causes damage to the tooth surface of the host, it is considered a cariogenic pathogen [2]. S. mutans produces acid through metabolism of a wide variety of carbohydrates, which can lower the pH down to pH 4 and causes demineralization of tooth enamel [3,4]. S. mutans has a well equipped acid defense system [5], it has growth advantages compared to other non-aciduric bacteria. In the acidic stage of the caries process, Lactobacilli and S. mutans become dominant [6]. S. mutans produces extracellular polysaccharides and surface adhesins that mediate its adherence and interaction with other microorganisms in the oral cavity [7,8]
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