title: The Rgg regulator of Streptococcus pyogenes influences utilization of nonglucose carbohydrates, prophage induction, and expression of the NAD-glycohydrolase virulence operon.
abstract: The expression of many virulence-associated genes in Streptococcus pyogenes is controlled in a growth phase-dependent manner. Unlike the model organisms Escherichia coli and Bacillus subtilis, such regulation is apparently not dependent upon alternative sigma factors but appears to rely on complex interactions among several transcriptional regulators, including Rgg. The purpose of this study was to identify changes in gene expression associated with inactivation of the rgg gene in S. pyogenes strain NZ131 (serotype M49). To this end, the transcriptomes of wild-type and rgg mutant strains were analyzed during both the exponential and postexponential phases of growth using Affymetrix NimbleExpress gene chips. Genomewide differences in transcript levels were identified in both phases of growth. Inactivation of rgg disrupted coordinate expression of genes associated with the metabolism of nonglucose carbon sources, such as fructose, mannose, and sucrose. The changes were associated with an inability of the mutant strain to grow using these compounds as the primary carbon source. Bacteriophage transcript levels were also altered in the mutant strain and were associated with decreased induction of at least one prophage. Finally, transcripts encoding virulence factors involved in cytolysin-mediated translocation of NAD-glycohydrolase, including the immunity factor IFS and the cytolysin (streptolysin O [SLO]), were more abundant in the mutant strain, which correlated with the amount of NADase and SLO activities in culture supernatant fluids. The results provide further evidence that Rgg contributes to growth phase-dependent gene regulation in strain NZ131.
authors.affiliation: Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Lee Medical Building, 414 East Clark Street, Vermillion, SD 57069-2390, USA.
authors.forename: Alexander V
authors.initials: AV
authors.lastname: Dmitriev
authors.forename: Emily J
authors.initials: EJ
authors.lastname: McDowell
authors.forename: Kyle V
authors.initials: KV
authors.lastname: Kappeler
authors.forename: Michelle A
authors.initials: MA
authors.lastname: Chaussee
authors.forename: Lindsey D
authors.initials: LD
authors.lastname: Rieck
authors.forename: Michael S
authors.initials: MS
authors.lastname: Chaussee
mesh_terms: D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology*; D050260:Carbohydrate Metabolism / Q000235:genetics*; D004268:DNA-Binding Proteins / Q000235:genetics / Q000502:physiology*; D003851:Deoxyribonucleases / Q000378:metabolism; D017353:Gene Deletion; D020869:Gene Expression Profiling; D015964:Gene Expression Regulation, Bacterial; D008562:Membrane Glycoproteins; D009244:NAD+ Nucleosidase / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D009876:Operon; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D021381:Protein Transport; D012329:RNA, Bacterial / Q000032:analysis / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis / Q000235:genetics; D013297:Streptococcus pyogenes / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism / Q000472:pathogenicity; D015534:Trans-Activators / Q000235:genetics / Q000502:physiology*; D037521:Virulence Factors / Q000096:biosynthesis*; D014775:Virus Activation / Q000235:genetics*
chemical_list: D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D012329:RNA, Bacterial; D012333:RNA, Messenger; D015534:Trans-Activators; D037521:Virulence Factors; D054353:Perforin; C074779:rgg protein, Streptococcus; D003851:Deoxyribonucleases; D009244:NAD+ Nucleosidase