Molecular Mechanism of Glucose Effect in E.coli.

研究发现，葡萄糖可降低大肠杆菌细胞内cAMP受体蛋白（CRP）的含量。在各种条件下生长的细胞中，CRP和β-半乳糖苷酶水平之间存在相关性。当通过操纵crp基因降低CRP浓度时，β-半乳糖苷酶的表达与CRP浓度成比例地降低，这些结果表明，葡萄糖引起的CRP浓度降低是分解代谢物抑制的主要因素之一。我们认为，葡萄糖通过降低细胞内CRP和cAMP水平引起分解代谢产物的抑制，并探讨了葡萄糖下调CRP的分子机制。将crp启动子替换为bla启动子主要消除了葡萄糖介导的crp表达调节。CRP结合位点II的破坏基本上消除了葡萄糖对CRP表达的下调。结论：CRP基因的自动调节回路在葡萄糖下调CRP中起关键作用。

It was found that glucose lowers the amount of cAMP receptor protein(CRP)inEscherichia coli cells. A correlation exists between CRP and b-galactosidase levels in cells growing under various conditions. When the CRP concentration is reduced by manipulating the crp gene, the b-galactosidase expression decreases in proportion to the concentration of CRP.These findings indicate that the lowered concentration of CRP caused by glucose is one of major factors for catabolite repression. We propose that glucose causes catabolite repression by lowering the intracellular levels of both CRP and cAMP.The molecular mechanism underlying the down-regulation of CRP by glucose was investigated. Replacement of the crp promoter to the bla promoter abolishes mostly the glucose-mediated regulation of crp expression. The disruption of the CRP-binding site II essentially eliminates the down-regulation of the crp expression by glucose. It was concluded that the autoregulatory circuit of the crp gene plays a key role in the down-regulation of CRP by glucose.