a Department of Biological Sciences, University of Delaware, Newark, Delaware 19711
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."
1 A portion of this work was submitted by one of us (S.B.) to the Department of Biological Sciences of the University of Delaware in partial fulfillment of the requirements for the Bachelor of Arts Degree, with distinction.
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