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Journal of Bacteriology logoLink to Journal of Bacteriology
. 1967 Jan;93(1):264–272. doi: 10.1128/jb.93.1.264-272.1967

Inducible System for the Utilization of β-Glucosides in Escherichia coli II. Description of Mutant Types and Genetic Analysis

S Schaefler a,1, W K Maas a
PMCID: PMC314997  PMID: 5335893

Abstract

Two types of mutants obtained by treating β-gl+ cells with nitrosoguanidine are described. One type, β-gl+c, is constitutive for the biosynthesis of the aryl β-glucoside splitting enzyme(s) and for the β-glucoside permease; the other (β-gl+sal) has lost the capacity to ferment salicin, but has retained the capacity to ferment arbutin and other aryl β-glucosides. By two successive mutational steps, β-gl+salc double mutants can be obtained. Determinations of the enzymatic splitting of salicin and p-nitrophenyl β-glucoside by β-gl+sal cells and extracts showed that these mutants have lost the capacity to split salicin but do split p-nitrophenyl β-glucoside; they possess the β-glucoside permease, and in them salicin is a gratuitous inducer for enzyme and permease biosynthesis. Studies on a β-gl+ strain, which splits salicin as well as p-nitrophenyl β-glucoside, have shown that the splitting of salicin is more temperature-sensitive than that of p-nitrophenyl β-glucoside and other β-glucosides. Other properties of the two activities are similar. Interrupted mating experiments and cotransduction with P1kc phage showed that the genetic determinants of the β-glucoside system map between the pyrE and ile loci. Three distinct mutational sites were found and are presumed to have the following functions: β-glA, a structural gene for an aryl β-glucoside splitting enzyme; β-glB, either the structural gene for the β-glucoside-permease or a regulatory gene; and β-glC, a regulatory gene (or site). Escherichia coli wild-type strains are of the genotype A+ B C+. The β-gl+ mutation determining the ability to ferment β-glucosides is considered to be a permease or regulatory mutation, and the resulting genotype is A+ B+ C+. The β-gl+sal phenotype results from a mutation in the β-glA gene (genotype A′ B+ C+), and the constitutive phenotype results from a mutation in the β-glC gene, the genotypes A+ B+Ca and A′ B+Ca corresponding to the phenotypes β-gl+c and β-gl+salc.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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