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Repression and induction of the nag regulon of Escherichia coll K‐12: the roles of nagC and nagA in maintenance of the uninduced state
Author(s) -
Plumbridge J. A.
Publication year - 1991
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1991.tb00828.x
Subject(s) - regulon , derepression , biology , operon , pep group translocation , repressor , gene , genetics , escherichia coli , psychological repression , biochemistry , microbiology and biotechnology , gene expression
Summary The nag regulon located at 15.5 min on the Escherichia coli chromosome consists of two divergent operons, nagE and nagBACD , encoding genes involved in the uptake and metabolism of N ‐acetylglucosamine. Null mutations have been created in each of the genes by insertion of antibiotic resistance cartridges. The phenotypes of the strains carrying the insertions in nagE, B and A were consistent with the previous identification of gene products: nagE , EII Nag , the N ‐acetylglucosamine specific transporter of the phosphotransferase system and nagB and nagA , the two enzymes necessary for the degradation of N ‐acetylglucosamine. Insertions in the napC result in derepression of the nag genes, which is consistent with earlier observations that the nagC gene encodes the repressor of the regulon. Insertions in nagA also provoke a derepression, implying that nagA has a role in the regulation of the expression of the nag regulon as well as in the degradation of the amino‐sugars. N ‐acetylglucosamine‐6‐phosphate, the intra‐cellular product of N‐acetylglucosamine transport and the substrate of the nagA gene product, is shown to be an inducer of the regulon and this suggests how nagA mutations result in derepression: the absence of N ‐acetylglucosamine‐6‐phosphate deacetylase allows N ‐acetylglucosamine‐6‐phosphate to accumulate and induce the regulon.