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缺乏环腺苷酸的大肠杆菌突变体中的分解代谢物阻遏

Catabolite repression in Escherichia coli mutants lacking cyclic AMP.

作者信息

Dessein A, Schwartz M, Ullmann A

出版信息

Mol Gen Genet. 1978 Jun 1;162(1):83-7. doi: 10.1007/BF00333853.

Abstract

The regulation of catabolite repression of beta-galactosidase has been studied in Escherichia coli mutants deleted for the adenyl cyclase gene (cya delta), and thus unable to synthesize cyclic AMP. It has been found that, provided a second mutation occurs either in the crp gene coding for the catabolite gene activator protein (CAP) or in the Lactose region, these mutants exhibit catabolite repression. If the catabolite repression seen in the mutant strains corresponds to the mechanism operating in wild-type cells the results would suggest that the intracellular concentration of cyclic AMP cannot be the unique regulator of catabolite repression.

摘要

已在缺失腺苷酸环化酶基因(cyaδ)因而无法合成环腺苷酸(cAMP)的大肠杆菌突变体中,研究了β-半乳糖苷酶的分解代谢物阻遏调控。现已发现,只要在编码分解代谢物基因激活蛋白(CAP)的crp基因或乳糖区域发生第二次突变,这些突变体就会表现出分解代谢物阻遏。如果在突变菌株中观察到的分解代谢物阻遏与在野生型细胞中起作用的机制相对应,那么结果将表明细胞内环腺苷酸的浓度不可能是分解代谢物阻遏的唯一调节因子。

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