Regulation of the β-Glucoside System in Escherchia coli K-12

Abstract

In Escherichia coli wild-type cells, a mutation at the β-glucoside regulatory gene (bglR⁺ to bglR⁻) leads to simultaneous expression of inducible phospho-β-glucosidase B (bglB⁺) and a β-glucoside-specific species of enzyme II (β-glucoside transport I [bglC⁺]); an additional mutation (bglS⁺ to bglS4) allows these enzymes to be formed constitutively. The bgl alleles have been mapped in the following order: pyrE, bglA, bglB, bglS, bglR, bglC, ilvD. The back mutation in the regulatory allele (bglR⁻ to bglR⁺) caused the cessation of the expression of the bglB⁺, bglS⁺ or bglS4, bglC⁺ alleles. However, a mutation in a strain with bglB⁺, bglS4, bglR8, bglC⁺ alleles, at the ini site that lies between the bglS4 and the bglR8 allele, allowed the expression of the bglS4 and bglB⁺ alleles, but showed no affect on the expression of the bglC⁺ allele. It is suggested that the ini mutation possesses a promotor-type function that in the absence of regulatory allele function (bglR8) renews the functioning of only the bglS4 and bglB⁺ alleles. The complementation studies have shown that the bglB⁺, bglS⁺ or bglS4, bglC⁺ alleles are expressed only in cis to the bglR⁻ allele. In the constitutive strain (bglB⁺, bglS4, bglR⁻, bglC⁺), the expressed bglS4 allele formed a soluble product that acts in trans over the bglB⁺ and bglC⁺ alleles and that appears effective only when the bglB⁺ and the bglC⁺ alleles are expressed in cis to the bglR⁻ allele. It thus showed that the constitutive biosynthesis of phospho-β-glucosidase B and β-glucoside transport I is under positive control. Since the regulatory allele bglR⁻ lies between the bglS4 and the blgC⁺ alleles, and acts in cis, it appears that the mutation (bglR⁺ to bglR⁻) allows the initiation of transcription in one direction to express the bglS4, bglB⁺ alleles and in the other to express the bglC⁺ allele. The structural genes bglB and bglC lie adjacent to the regulatory genes bglR and bglS, and the structural genes are coordinately controlled by the regulatory genes. It is, therefore, proposed that the bglB, bglS, bglR, bglC genes form a bgl operon.