Catabolite repression of β-galactosidase synthesis in Escherichia coli

Abstract

Repression by glucose of [beta]-galactosidase synthesis is spontaneously reversible in all strains of E. coli examined long before the glucose has all been consumed. The extent of recovery and the time necessary for reversal differ among various strains. Other inducible enzymes show similar effects. This transient effect of glucose repression is observed in constitutive (i-) and permease-less (y-) cells as well as in the corresponding i+ and y+ strains. Repression is exerted by several rapidly metabolizable substrates (galactose, ribose and ribonucleosides) but not by non-metabolized or poorly metabolized compounds (2-deoxyglucose, 2-deoxyribose, phenyl thio-[beta]-galactoside and 2-deoxyribonucleosides). The transient repression with glucose is observed in inducible cells supplied with a powerful inducer of [beta]-galsctosidase synthesis (e.g isoprppyl thio-[beta]-galactoside) but not with a weak inducer (lactose); in the latter instance glucose repression is permanent. Diauxic growth on glucose plus lactose can be abolished by including isopropyl thio-[beta]-galactoside in the medium. In some strains phosphate starvation increases catabolite repression; in others it relieves it. Adenine stravation in an adenine-requiring mutant also relieves catabolite repression by glycerol but not that by glucose. Restoration of phosphate or adenine to cells starved of these nutrients causes a pronounced temporary repression. Alkaline-phosphatase synthesis is not affected by the availability of adenine. During periods of transient repression of induced anzyme synthesis the differential rate of ribonu-cleic-acid (RNA) synthesis, measured by labelled uracil incorporation in 2 min. pulses, shows a temporary rise. The differential rate of uracil incorporation into RNA falls during exponential growth of batch cultures of E. coli. This is equally true for uracil-requiring and non-requiring strains. The fall in the rate of incorporation has been shown to be due to a real fall in the rate of RNA synthesis. The significance of the changes in the rate of RNA synthesis is discussed. A partial model of catabolite repression is presented with suggestions for deter-mining the chemical identification of the catabolite co-repressor itself.