Abstract
Acute transient catabolite repression of [beta]-galactosidase synthesis, observed when glucose is added to glycerol-grown cells of E coli (Moses & Prevost, 1966), requires the presence of a functional operator gene (o) in the lactose operon. Total deletion of the operator gene abolished acute transient repres -sion, even in the presence of a functional regulator gene (i). Regulator constitutives (i-) also snow transient repression provided that the operator gene is functional. Regulator deletion mutants (idel), with which to test specifically the role of the i f ene, have not so far been available. The above mutants, showing various changes in the lactose operon, show no alteration in the effect of glucose on induced trypto-phanase synthesis. Glucose metabolism, as measured in terms of the release of 14CO2 from [1-14C] glucose and [6-14C] glucose, also showed no differences between strains exhibiting or not exhibiting transient repression. This suggests no change in the operation of the pentose phosphate cycle, a metabolic activity known to be of paramount importance for glucose repression of [beta]-galactosidase synthesis (Prevost & Moses, 1967). Chronic permanent repression by glucose of [beta]-galactosidase synthesis (less severe in degree than acute transient repression) persists in strains in which transient repression has been genetically abolished. Constitutive alkaline-phosphatase synthesis, which shows no transient repression, also demonstrates chronic permanent repression by glucose. Chlor-amphenicol repression also persists in mutants with no transient repression, and also affects alkaline phosphatase. It is suggested that chronic permanent repression and chloramphenical repression are non-specific, and that they do not influence [beta] -galactosidase synthesis via the regulatory system of the lactose operon.