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首页> 外文期刊>Journal of bacteriology >d-Fucose as a Gratuitous Inducer of the l-Arabinose Operon in Strains of Escherichia coli B/r Mutant in Gene araC
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d-Fucose as a Gratuitous Inducer of the l-Arabinose Operon in Strains of Escherichia coli B/r Mutant in Gene araC

机译:d-岩藻糖作为araC基因突变株中大肠杆菌B / r突变株l-阿拉伯糖操纵子的无偿诱导物

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摘要

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.”
机译:d-岩藻糖是l-阿拉伯糖的不可代谢的类似物,可通过抑制l-阿拉伯糖操纵子的诱导,阻止大肠杆菌B / r在矿物盐介质和l-阿拉伯糖上的生长。突变导致基因 araC 中的d-岩藻糖抗性图谱,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也允许d-岩藻糖充当免费的诱导物。结论是耐d-岩藻糖的突变体产生诱导子特异性改变的 araC 基因产物。在由免费诱导物d-岩藻糖诱导的细胞中添加l-阿拉伯糖会导致操纵子表达的严重瞬时抑制,然后永久性分解代谢物抑制。当使用不能代谢1-阿拉伯糖的细胞时,获得了短暂的抑制,但没有永久的分解代谢物抑制。结论是,单独运输1-阿拉伯糖足以实现其自身操纵子的瞬时阻遏,但是必须实现1-阿拉伯糖的代谢才能实现对1-阿拉伯糖操纵子的永久分解代谢物的阻抑。这种一般效果被称为“自分解代谢物抑制”。

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