d -Fucose as a Gratuitous Inducer of the l -Arabinose Operon in Strains of Escherichia coli B/r Mutant in Gene araC

Abstract

d -Fucose, a nonmetabolizable analogue of l -arabinose, prevents growth of Escherichia coli B/r on a mineral salts medium plus l -arabinose by inhibiting induction of the l -arabinose operon. Mutations giving rise to d -fucose resistance map in gene araC and result in constitutive expression of the l -arabinose operon. Most of these mutations also permit d -fucose to serve as a gratuitous inducer. It is concluded that d -fucose-resistant mutants produce an araC gene product with an altered inducer specificity. Addition of l -arabinose to cells induced with the gratuitous inducer, d -fucose, resulted in severe transient repression of operon expression followed by permanent catabolite repression. Transient repression but no permanent catabolite repression was obtained when cells unable to metabolize l -arabinose were employed. It is concluded that transport of l -arabinose alone is sufficient to achieve transient repression of its own operon, but that metabolism of l -arabinose must occur to achieve permanent catabolite repression of the l -arabinose operon. This general effect has been termed “self-catabolite repression.”