Beverin S, Sheppard D E, Park S S
J Bacteriol. 1971 Jul;107(1):79-86. doi: 10.1128/jb.107.1.79-86.1971.
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."
D-岩藻糖是L-阿拉伯糖的一种不可代谢类似物,它通过抑制L-阿拉伯糖操纵子的诱导,阻止大肠杆菌B/r在矿物盐培养基加L-阿拉伯糖上生长。导致对D-岩藻糖抗性的突变定位在araC基因中,并导致L-阿拉伯糖操纵子的组成型表达。这些突变中的大多数还使D-岩藻糖能够作为一种安慰诱导物。得出的结论是,对D-岩藻糖抗性的突变体产生了一种诱导物特异性改变的araC基因产物。向用安慰诱导物D-岩藻糖诱导的细胞中添加L-阿拉伯糖,导致操纵子表达严重的瞬时抑制,随后是永久性的分解代谢物阻遏。当使用不能代谢L-阿拉伯糖的细胞时,获得了瞬时抑制但没有永久性的分解代谢物阻遏。得出的结论是,仅L-阿拉伯糖的转运就足以实现其自身操纵子的瞬时抑制,但L-阿拉伯糖的代谢必须发生才能实现L-阿拉伯糖操纵子的永久性分解代谢物阻遏。这种普遍效应被称为“自我分解代谢物阻遏”。