Expression of the chitobiose operon of Escherichia coli is regulated by three transcription factors: NagC, ChbR and CAP

• Published in: Molecular microbiology 2004-04, Vol.52 (2), p.437-449
• Main Authors: Plumbridge, Jacqueline, Pellegrini, Olivier
• Format: Article
• Language: English
• Subjects: Bacteriology; Biological and medical sciences; Chitin - metabolism; Cyclic AMP Receptor Protein; Disaccharides - metabolism; DNA Footprinting; Escherichia coli; Escherichia coli - enzymology; Escherichia coli - genetics; Escherichia coli Proteins - genetics; Escherichia coli Proteins - metabolism; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Bacterial; Microbiology; Miscellaneous; Molecular Sequence Data; Mutation; Operon; Plasmids; Promoter Regions, Genetic; Receptors, Cell Surface - genetics; Receptors, Cell Surface - metabolism; Recombination, Genetic; Repressor Proteins - genetics; Repressor Proteins - metabolism; RNA, Bacterial - isolation & purification; RNA, Bacterial - metabolism; Transcription Factors - genetics; Transcription Factors - metabolism
• ISSN: 0950-382X; 1365-2958
• DOI: 10.1111/j.1365-2958.2004.03986.x

Summary The chitobiose operon, chbBCARFG, encodes genes for the transport and degradation of the N‐acetylglucosamine disaccharide, chitobiose. Chitobiose is transported by the phosphotransferase system (PTS) producing chitobiose‐6P which is hydrolysed to GlcNAc‐6P by the chbF gene product and then further degraded by the nagBA gene products. Expression of the chb operon is repressed by NagC, which regulates genes involved in amino sugar metabolism. The inducer for NagC is GlcNAc‐6P. NagC binds to two sites separated by 115 bp and the transcription start point of the chb operon lies within the downstream NagC operator. In addition the chb operon encodes its own specific regulator, ChbR, an AraC‐type dual repressor–activator, which binds to two direct repeats of 19 bp located between the two NagC sites. ChbR is necessary for transcription activation in the presence of chitobiose in vivo. Induction of the operon also requires CAP, which binds to a site upstream of the ChbR repeats. In the absence of chitobiose both NagC and ChbR act as repressors. Together these three factors cooperate in switching chb expression from the repressed to the activated state. The need for two specific inducing signals, one for ChbR to activate the expression of the operon and a second for NagC to relieve its repression, ensure that the chb operon is only induced when there is sufficient flux through the combined chb‐nag metabolic pathway to activate expression of both the chb and nag operons.