Multiple regulators control expression of the Entner-Doudoroff aldolase (Eda) of Escherichia coli
Multiple regulators control expression of the Entner-Doudoroff aldolase (Eda) of Escherichia coli
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DOI：
10.1128/jb.187.3.991-1000.2005
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发表时间：
2005-02-01
影响因子：
3.2
通讯作者：
Conway, T
中科院分区：
文献类型：
--
作者：
Murray, EL;Conway, T
编码Entner-Doudoroff醛缩酶的大肠杆菌eda基因是几种糖酸催化的核心。在这里，我们表明，埃达的合成是由葡萄糖酸盐，葡萄糖醛酸盐，或甲基-β-D-葡萄糖醛酸;磷酸盐限制和碳饥饿的增长。eda的转录起始于三个启动子，命名为P1、P2和P4，每个启动子负责在不同生长条件下的诱导。P1控制葡萄糖酸盐对eda的诱导，并受GntR调节。P2控制葡萄糖醛酸和半乳糖醛酸的eda诱导，并由KdgR调节。P4在磷酸盐饥饿的条件下是活跃的，并直接由PhoB控制。此外，CsrA激活Eda合成，显然是通过间接机制，该机制可能涉及与碳饥饿相关的表达水平的适度变化。eda的复杂的调节进行了讨论，就其几个生理作用，这显然不仅容纳糖酸催化剂，但也解毒代谢物，可以积累在饥饿诱导的压力。
The Escherichia coli eda gene, which encodes the Entner-Doudoroff aldolase, is central to the catabolism of several sugar acids. Here, we show that Eda synthesis is induced by growth on gluconate, glucuronate, or methyl-p-D-glucuronide; phosphate limitation; and carbon starvation. Transcription of eda initiates from three promoters, designated P1, P2, and P4, each of which is responsible for induction under different growth conditions. P1 controls eda induction on gluconate and is regulated by GntR. P2 controls eda induction on glucuronate and galacturonate and is regulated by KdgR. P4 is active under conditions of phosphate starvation and is directly controlled by PhoB. In addition, CsrA activates Eda synthesis, apparently by an indirect mechanism that may be involved in the modest changes in expression level that are associated with carbon starvation. The complex regulation of eda is discussed with respect to its several physiological roles, which apparently accommodate not only sugar acid catabolism but also detoxification of metabolites that could accumulate during starvation-induced stress.