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Kaufman, GE and Yother, J (2007) CcpA-dependent and -independent control of beta-galactosidase expression in Streptococcus pneumoniae occurs via regulation of an upstream phosphotransferase system-encoding operon. J. Bacteriol. 189:5183-92


A spontaneous mutant of Streptococcus pneumoniae strain D39 exhibiting elevated beta-galactosidase activity was identified. We determined that the beta-galactosidase activity was due to BgaA, a surface protein in S. pneumoniae, and that the expression of bgaA was regulated. Transcription analyses demonstrated expression of bgaA in the constitutive beta-galactosidase (BgaA(C)) mutant, but not in the parent. beta-Galactosidase expression was induced in the parent under specific growth conditions; however, the levels did not reach those of the BgaA(C) mutant. We localized the mutation resulting in the BgaA(C) phenotype to a region upstream of bgaA and in the promoter of a phosphoenolpyruvate-dependent phosphotransferase system (PTS) operon. The mutation was in a catabolite-responsive element (cre) and affected the binding of CcpA (catabolite control protein A), a key regulator of many carbon metabolism genes. The pts operon and bgaA were cotranscribed, and their transcription was regulated by CcpA. Deletion of ccpA altered beta-galactosidase activity, leading to a sevenfold increase in the parent but a fivefold decrease in the BgaA(C) mutant. The resulting beta-galactosidase activities were the same in the two strains, suggesting the presence of a second repressor. The presence of glucose in the growth medium resulted in pts-bgaA repression by both CcpA and the second repressor, with the latter being important in responding to the glucose concentration. Expression of beta-galactosidase is important for S. pneumoniae adherence during colonization of the nasopharynx, a site normally devoid of glucose. CcpA and environmental glucose concentrations thus appear to play important roles in the regulation of a niche-specific virulence factor.


PubMed PMC1951873 Online version:10.1128/JB.00449-07


Bacterial Proteins/genetics; Bacterial Proteins/metabolism; Bacterial Proteins/physiology; Base Sequence; DNA-Binding Proteins/genetics; DNA-Binding Proteins/metabolism; DNA-Binding Proteins/physiology; Electrophoretic Mobility Shift Assay; Gene Deletion; Gene Expression Regulation, Bacterial/drug effects; Glucose/pharmacology; Molecular Sequence Data; Mutation; Operon; Phosphoenolpyruvate Sugar Phosphotransferase System/genetics; Phosphoenolpyruvate Sugar Phosphotransferase System/metabolism; Promoter Regions, Genetic; Protein Binding; Repressor Proteins/genetics; Repressor Proteins/metabolism; Repressor Proteins/physiology; Streptococcus pneumoniae/genetics; Streptococcus pneumoniae/growth & development; Streptococcus pneumoniae/metabolism; Transcription, Genetic; beta-Galactosidase/genetics; beta-Galactosidase/metabolism



Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status


GO:0010944: negative regulation of transcription by competitive promoter binding



Figure 4A: Which describes the negative regulation of B-galactosidase via the ccpa protein in Streptococcus pneumoniae strain D39 serotype 2. In the control, the deletion of catabolite control protein A (ccpa) resulted in an increase in the transcript levels of bga and pts. In the the BgaAC mutant, a decrease in transcription occurred for both bga and pts.

Figure 5: Showing that the D39 pts promoter expressed a higher affinity for the CcpA protein rather than the second repressor. The BgaAC mutant bacteria with its pts promoter expressed the higher affinity for the second repressor.

CACAO 12321


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