Comparative genome hybridization of <i>Streptococcus mutans</i> strains

Waterhouse, Janet C.; Swan, Daniel; Russell, R. R. B.

doi:10.1111/j.1399-302x.2007.00330.x

Cited by 45 publications

(49 citation statements)

References 38 publications

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“…We found that genes within three different genomic islands were differentially regulated in the clpP mutant (Table 1). Among them were two genomic islands, TnSmu1 and TnSmu2, whose distribution among the different isolates had been previously studied (50,51). TnSmu1 corresponds to a large region of 23 kb spanning from SMU.191 to SMU.226 (50,51).…”

Section: Resultsmentioning

confidence: 99%

ClpP of Streptococcus mutans Differentially Regulates Expression of Genomic Islands, Mutacin Production, and Antibiotic Tolerance

et al. 2010

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Streptococcus mutans is the primary etiological agent of human dental caries and, at times, of infective endocarditis. Within the oral cavity, the pathogen is subjected to conditions of stress. A well-conserved protein complex named ClpP (caseinolytic protease) plays a vital role in adaptation under stress conditions. To gain a better understanding of the global role of the ClpP protease in cellular homeostasis, a transcriptome analysis was performed using a ⌬clpP mutant strain. The expression levels of more than 100 genes were up-or downregulated in the ⌬clpP mutant compared to the wild type. Notably, the expression of genes in several genomic islands, such as TnSmu1 and TnSmu2, was differentially modulated in the ⌬clpP mutant strain. ClpP deficiency also increased the expression of genes associated with a putative CRISPR locus. Furthermore, several stress-related genes and genes encoding bacteriocin-related peptides and many transcription factors were also found to be altered in the ⌬clpP mutant strain. A comparative analysis of the two-dimensional protein profile of the wild type and the ⌬clpP mutant strains showed altered protein profiles. Comparison of the transcriptome data with the proteomic data identified four common gene products, suggesting that the observed altered protein expression of these genes could be due to altered transcription. The results presented here indicate that ClpP-mediated proteolysis plays an important global role in the regulation of several important traits in this pathogen.

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Section: Resultsmentioning

confidence: 99%

ClpP of Streptococcus mutans Differentially Regulates Expression of Genomic Islands, Mutacin Production, and Antibiotic Tolerance

et al. 2010

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“…They constitute the dispensable genome, while those genes shared by all strains within a species are regarded as the core genome. In S. mutans, comparison of the genome sequences of strains UA159 and NN2025 revealed that these two strains differ in 10% of the genes (47), while 20% of the open reading frames (ORFs) in strain UA159 have been estimated to belong to the dispensable genome by a DNA hybridization-based comparison with nine other strains (83). In addition, comparative genome hybridization of 11 strains showed that 16.6% of the ORFs included in the microarray were missing in at least one of the genomes (89).…”

Section: Discussionmentioning

confidence: 99%

Distribution of Putative Virulence Genes in Streptococcus mutans Strains Does Not Correlate with Caries Experience

Argimón

Caufield

2011

J Clin Microbiol

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Streptococcus mutans, a member of the human oral flora, is a widely recognized etiological agent of dental caries. The cariogenic potential of S. mutans is related to its ability to metabolize a wide variety of sugars, form a robust biofilm, produce copious amounts of lactic acid, and thrive in the acid environment that it generates. The remarkable genetic variability present within the species is reflected at the phenotypic level, notably in the differences in the cariogenic potential between strains. However, the genetic basis of these differences is yet to be elucidated. In this study, we surveyed by PCR and DNA hybridization the distribution of putative virulence genes, genomic islands, and insertion sequences across a collection of 33 strains isolated from either children with severe early childhood caries (S-ECC) or those who were caries free (CF). We found this genetically diverse group of isolates to be remarkably homogeneous with regard to the distribution of the putative virulence genes and genetic elements analyzed. Our findings point to the role of other factors in the pathogenesis of S-ECC, such as uncharacterized virulence genes, differences in gene expression and/or enzymatic activity, cooperation between S. mutans strains or with other members of the oral biota, and host factors.

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“…Likewise, irvA induction has also been found to be associated with several other genetic mutations known to have multiple stress-and virulence-related phenotypes (40). Moreover, irvA has thus far been detected in numerous strains of S. mutans (1,25,42); therefore, it may be a fundamental component of the basic machinery utilized to modulate multiple virulence-associated functions required for persistence.…”

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Characterization of irvR , a Novel Regulator of the irvA -Dependent Pathway Required for Genetic Competence and Dextran-Dependent Aggregation in Streptococcus mutans

et al. 2008

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Previous studies identified irvA as a normally repressed but highly inducible transcription regulator capable of repressing mutacin I gene expression in Streptococcus mutans. In this study, we aimed to identify and characterize the regulator(s) responsible for repressing the expression of irvA. An uncharacterized open reading frame (SMU.1398) located immediately adjacent to irvA and annotated as a putative transcription repressor was identified as a likely candidate. The results of mutation studies confirmed that the expression of irvA was greatly increased in the SMU.1398 background. Mutation of SMU.1398 ("irvR") abolished genetic competence and reduced the expression of the late competence genes/operons comEA, comY, and dprA without affecting the expression of the known competence regulators comC, comED, or comX. In addition, irvR was found to be a potent negative regulator of dextran-dependent aggregation (DDAG) and gbpC expression. Each of these irvR mutant phenotypes could be rescued with a double mutation of irvA or complemented by introducing a wild-type copy of irvR on a shuttle vector. These data indicate that the repression of irvA is critically dependent upon irvR and that irvA repression is essential for the development of genetic competence and the proper control of DDAG in S. mutans.Streptococcus mutans is a gram-positive oral commensal species found in human dental plaque and is primarily associated with the initiation of caries development (tooth decay) (3,8,28,30,38, 41,45). Certain species, such as S. mutans, have a much greater capacity to both excrete acidic metabolites (acidogenic) and proliferate in an acidic environment (aciduric) and thus, can gain a competitive advantage over nonaciduric species (2,29). Yet, examinations of oral plaque samples and carious lesions have identified numerous other aciduric species (4, 9), which suggests that the success of S. mutans as a dental pathogen cannot be solely attributed to its acid tolerance. Biofilm formation, natural competence, and bacteriocin production are also recognized as virulence factors that are necessary for the persistence of S. mutans in the presence of numerous environmental stresses and fierce interspecies competition (2,21,29).Studies of genetic factors that regulate these processes in S. mutans have found a surprising variety of genetic mutations that each affect multiple virulence factors and stress tolerances simultaneously (7, 14-18, 20, 22-24, 26, 33, 36, 39, 43). This implies that a large overlap must exist between the pathways responsible for the regulation of persistence-related abilities. For example, our laboratory and others have observed that a mutation in the S. mutans ortholog of luxS creates altered oxidative and acid stress tolerances, as well as defects in biofilm formation, natural competence, and bacteriocin (mutacin I) production. (25-27, 37, 43, 44).Previously, our laboratory further investigated the mutacin

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Comparative genome hybridization of Streptococcus mutans strains

Cited by 45 publications

References 38 publications

ClpP of Streptococcus mutans Differentially Regulates Expression of Genomic Islands, Mutacin Production, and Antibiotic Tolerance

ClpP of Streptococcus mutans Differentially Regulates Expression of Genomic Islands, Mutacin Production, and Antibiotic Tolerance

Distribution of Putative Virulence Genes in Streptococcus mutans Strains Does Not Correlate with Caries Experience

Characterization of irvR , a Novel Regulator of the irvA -Dependent Pathway Required for Genetic Competence and Dextran-Dependent Aggregation in Streptococcus mutans

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