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Research Article 15: On the Mechanism of Catabolite Repression

G. Contesse, M. Crépin, F. Gros, A. Ullmann, J. Monod


It has long been established that the presence of glucose or of an actively metabolizable carbon source inhibits the synthesis of certain bacterial enzymes, a situation usually referred to as catabolite repression. In spite of considerable work devoted to this phenomenon, little is known about its molecular mechanism.

Experiments by Nakada and Magasanik (1964), Loomis and Magasanik (1967), Tyler and Magasanik (1969) and by Jacquet and Kepes (1969) strongly support the idea that catabolite repression affects gene expression at the transcriptional rather than at the translational level. Moreover, studies by Pastan and Perlman (1968), Perlman et al. (1969), and Silverstone et al. (1969) indicate that certain mutations within the promoter site of the lac operon generate almost complete resistance to catabolite repression, which one would tend to interpret as showing that initiation of message synthesis is the sensitive step.

Involvement of 3′,5′ cyclic AMP in these phenomena was first suggested by work by Makman and Sutherland (1965) indicating that E. coli cells grown in the presence of glucose as a carbon source contain less of this nucleotide than cells maintained in milder repressing conditions. Quite significantly, it was shown by Ullmann and Monod (1968) and Perlman and Pastan (1968) that the presence of 3′,5′ cyclic AMP almost completely overcomes the transient or permanent glucose effect on β-galactosidase synthesis.

In this paper we wish to describe some experiments aimed at obtaining more information on the target and molecular mechanism of the catabolite effect.

Our results confirm that catabolite repression operates at...

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