Gendron R P, Sheppard D E
J Bacteriol. 1974 Feb;117(2):417-21. doi: 10.1128/jb.117.2.417-421.1974.
Two independent mutants resistant to l-arabinose inhibition only in the presence of d-glucose were isolated from an l-arabinose-sensitive strain containing the araD139 mutation. Preliminary mapping studies indicate that these mutations are closely linked to the araIOC region. Addition of d-glucose to growing cultures of these mutants results in a 95 to 98% repression of ara operon expression, as compared to a 50% repression of the parental control. Since cultures of both mutant and parental strains undergo a 50% repression of lac operon expression upon addition of glucose, the hypersensitivity to catabolite repression exhibited by these mutants is specific for the ara operon. Addition of cyclic adenosine monophosphate reverses the catabolite repression of the ara operon in both mutant and parent strains to 70 to 80% of the control. It is suggested that in these mutants the affinity of the ara operon initiator region for the cAMP-catabolite-activator protein complex may have been altered.
从含有araD139突变的L-阿拉伯糖敏感菌株中分离出两个仅在D-葡萄糖存在时对L-阿拉伯糖抑制具有抗性的独立突变体。初步定位研究表明,这些突变与araIOC区域紧密连锁。与亲本对照的50%阻遏相比,向这些突变体的生长培养物中添加D-葡萄糖会导致ara操纵子表达受到95%至98%的阻遏。由于在添加葡萄糖后,突变体菌株和亲本菌株的培养物中lac操纵子表达均受到50%的阻遏,因此这些突变体对分解代谢物阻遏的超敏感性是ara操纵子特有的。添加环磷酸腺苷可使突变体菌株和亲本菌株中ara操纵子的分解代谢物阻遏恢复到对照的70%至80%。有人提出,在这些突变体中,ara操纵子起始区域对cAMP-分解代谢物激活蛋白复合物的亲和力可能发生了改变。