Inducibility of β-Glucuronidase in Wild-Type and Hexuronate-Negative Mutants of Escherichia coli K-12

Abstract

In strain K-12 of Escherichia coli , β-glucuronidase synthesis was induced only by β-glucuronides: all intermediates of the hexuronate pathway able to enter the cells failed to induce the enzyme significantly. The induction pattern of β-glucuronidase clearly differentiates the mode of regulation of its synthesis from those of the subsequent enzymes of the pathway, which are induced by fructuronate and/or tagaturonate. In mutant strains blocked in glucuronate metabolism after the isomerase step, β-glucuronidase synthesis was still induced by a β-glucuronide. Glucuronate and fructuronate, which are accumulated and mutually interconverted within the cells, become good inducers of β-glucuronidase: they induce up to a level one-half that obtained in the wild-type strain in the presence of β-glucuronide alone. In an isomerase-negative strain where fructuronate is not produced, β-glucuronidase was no longer induced by β-glucuronide unless supplemented with fructuronate. In this strain, glucuronate alone or fructuronate alone exhibited greater inducing ability than in the wild-type strain. Moreover, fructuronate could also enhance glucuronate-induced synthesis of β-glucuronidase. Glucuronate was not able to activate β-glucuronideinduced synthesis of β-glucuronidase. Therefore, the induction of β-glucuronidase synthesis depends upon two factors which, when acting separately, are both poor inducers but can act cooperatively; one factor is β-glucuronide or glucuronate and the second is fructuronate. The specific inducing capacity of each of these three compounds as well as the hypothetical mechanism(s) of the action of fructuronate are discussed.