Control of acid resistance in Escherichia coli
Control of acid resistance in Escherichia coli
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DOI：
10.1128/jb.181.11.3525-3535.1999
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发表时间：
1999-06-01
影响因子：
3.2
通讯作者：
Foster, JW
中科院分区：
文献类型：
--
作者：
Castanie-Cornet, MP;Penfound, TA;Foster, JW
大肠杆菌的耐酸性（AR）被定义为耐受pH 2.5或更低的酸挑战的能力，并且通常仅限于稳定期细胞的性状。早期的报道描述了E.杆菌在本研究中，这三个系统的遗传学和控制已经被更清楚地定义，第一个AR系统（指定为氧化或葡萄糖抑制的AR系统）的表达先前被证明需要替代的σ因子RpoS。与葡萄糖阻遏一致，该系统也被证明在许多情况下依赖于环AMP受体蛋白。第二个AR系统需要在pH 2.5酸挑战期间添加精氨酸、精氨酸脱羧酶的结构基因（adiA）和调节剂cysB，这证实了早期的报道。第三个AR系统需要谷氨酸在pH 2.5时提供保护，这是编码谷氨酸脱羧酶（gadA或gadB）的两个基因之一，以及编码推定的谷氨酸：γ-氨基丁酸反向转运蛋白（gadC）的基因。在pH 2.5时，仅需要两种谷氨酸脱羧酶中的一种来进行保护。然而，在pH 2的生存需要两种谷氨酸脱羧酶同工酶。GAD基因的稳定期和酸性pH调节被证明是可分离的。gadA和gadB的稳定相诱导需要由rpoS编码的替代sigma因子sigma（S）。然而，这些酶的酸诱导，这被证明发生在指数期和静止期细胞，被证明是sigma（S）的独立性。两种gad基因都不需要挥发性脂肪酸的诱导。数据还表明，AR通过氨基酸脱羧酶系统需要的不仅仅是诱导型脱羧酶和反向转运蛋白。另一个令人惊讶的发现是，最初被认为是酸诱导的σ（S）依赖性氧化系统实际上被证明在进入固定相后被诱导，而与pH无关。然而，在pH 8下产生的抑制剂以某种方式干扰该系统的活性，产生酸诱导的错觉。结果还表明，在复合培养基（Luria-Bertani肉汤或脑心浸液肉汤加0.4%葡萄糖）中，在pH 2时提供最有效保护的AR系统是谷氨酸依赖性GAD系统。因此，E.大肠杆菌具有三个重叠的酸存活系统，其不同水平的控制和对活性的不同要求确保至少一个系统可用于在天然存在的酸性环境下保护静止期细胞。
Acid resistance (AR) in Escherichia coli is defined as the ability to withstand an acid challenge of pH 2.5 or less and is a trait generally restricted to stationary-phase cells. Earlier reports described three AR systems in E. coli. In the present study, the genetics and control of these three systems have been more clearly defined, Expression of the first AR system (designated the oxidative or glucose-repressed AR system) was previously shown to require the alternative sigma factor RpoS. Consistent with glucose repression, this system also proved to be dependent in many situations on the cyclic AMP receptor protein. The second AR system required the addition of arginine during pH 2.5 acid challenge, the structural gene for arginine decarboxylase (adiA), and the regulator cysB, confirming earlier reports. The third AR system required glutamate for protection at pH 2.5, one of two genes encoding glutamate decarboxylase (gadA or gadB), and the gene encoding the putative glutamate:gamma-aminobutyric acid antiporter (gadC). Only one of the two glutamate decarboxylases was needed for protection at pH 2.5. However, survival at pH 2 required both glutamate decarboxylase isozymes. Stationary phase and acid pH regulation of the gad genes proved separable. Stationary-phase induction of gadA and gadB required the alternative sigma factor sigma(S) encoded by rpoS. However, acid induction of these enzymes, which was demonstrated to occur in exponential- and stationary-phase cells, proved to be sigma(S) independent. Neither gad gene required the presence of volatile fatty acids for induction. The data also indicate that AR via the amino acid decarboxylase systems requires more than an inducible decarboxylase and antiporter. Another surprising finding was that the sigma(S)-dependent oxidative system, originally thought to be acid induced, actually proved to be induced following entry into stationary phase regardless of the pH, However, an inhibitor produced at pH 8 somehow interferes with the activity of this system, giving the illusion of acid induction. The results also revealed that the AR system affording the most effective protection at pH 2 in complex medium (either Luria-Bertani broth or brain heart infusion broth plus 0.4% glucose) is the glutamate-dependent GAD system. Thus, E. coli possesses three overlapping acid survival systems whose various levels of control and differing requirements for activity ensure that at least one system will be available to protect the stationary-phase cell under naturally occurring acidic environments.