CRYPTIC OPERON FOR BETA-GLUCOSIDE METABOLISM IN ESCHERICHIA-COLI-K12 - GENETIC-EVIDENCE FOR A REGULATORY PROTEIN

Abstract

E. coli K12 does not metabolize .beta.-glucosides such as arbutin and salicin because of lack of expression of the bglBSRC operon, which contains structural genes for transport (bglC) and hydrolysis (bglB) of phospho-.beta.-glucosides. Mutants carrying lesions in the cis-acting regulatory site bglR metabolize .beta.-glucosides as a consequence of expression of this cryptic operon. Mutations promoting .beta.-glucoside metabolism unlinked to bglR were isolated; some of these were amber mutations. All of them were mapped at 27 min on the E. coli K12 linkage map and appeared to define a single gene, for which the designation bglY is proposed. Utilization of .beta.-glucosides in bglY mutants appeared to be a consequence of expression of the bglBSRC operon, since bglB bglR and bglB bglY double mutants had the same phenotype. All bglY mutations analyzed were recessive to the wild-type bglY+ allele. Phospho-.beta.-glucosidase B and .beta.-glucoside transport activities are inducible in bglY mutants, as they are in bglR mutants. Metabolism of .beta.-glucosides in both bglR and bglY mutants required cAMP. bglY appears to encode a protein acting as a repressor of the bglBSRC operon, active in both the presence and absence of .beta.-glucosides, whose recognition site would be within the bglR locus.