Iuchi S, Aristarkhov A, Dong J M, Taylor J S, Lin E C
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
J Bacteriol. 1994 Mar;176(6):1695-701. doi: 10.1128/jb.176.6.1695-1701.1994.
Expression of sdhCDAB (encoding succinate dehydrogenase) and lctD (encoding the flavin-linked L-lactate dehydrogenase) is elevated aerobically and repressed anaerobically in Escherichia coli. The repression is initiated by autophosphorylation of the sensor protein ArcB, followed by phosphoryl group transfer to the regulator ArcA. ArcA-P, a global transcriptional regulator, then prevents sdh and lct expression. The stimulus for ArcB is not O2 deficiency per se. In vitro experiments showed that ArcB phosphorylation is enhanced by pyruvate, D-lactate, acetate, and NADH, the concentrations of which are likely to increase with the lack of an effective exogenous electron sink. In addition to their aerobic function, the two primary dehydrogenases also have roles in anaerobic nitrate respiration. Results presented here indicate that the increase of sdh and lct expression by nitrate depended on its chemical reduction, which in turn diminished the ArcA-P pool. Unexpectedly, a mutation in the fnr gene (encoding a global regulator involved in anaerobic metabolism) also alleviated the anaerobic repressions. Mutations in arcB or arcA were epistatic over that of fnr. Moreover, since this relief was counteracted by pyruvate in the growth medium, Fnr appears to affect formation of stimuli for ArcB. It is possible that Fnr also indirectly affects some of the other members of the arcA modulon, e.g., cyoABCDE (encoding the cytochrome o complex), cydAB (encoding the cytochrome d complex), and sodA (encoding the manganese-dependent superoxide dismutase).
在大肠杆菌中,编码琥珀酸脱氢酶的sdhCDAB和编码黄素连接的L-乳酸脱氢酶的lctD的表达在需氧条件下升高,而在厌氧条件下受到抑制。这种抑制是由传感蛋白ArcB的自磷酸化引发的,随后磷酸基团转移至调节因子ArcA。全局转录调节因子ArcA-P随后会阻止sdh和lct的表达。ArcB的刺激因素并非氧气缺乏本身。体外实验表明,丙酮酸、D-乳酸、乙酸和NADH会增强ArcB的磷酸化,而随着有效的外源电子受体的缺乏,这些物质的浓度可能会增加。除了其需氧功能外,这两种主要的脱氢酶在厌氧硝酸盐呼吸中也发挥作用。此处给出的结果表明,硝酸盐导致的sdh和lct表达增加依赖于其化学还原作用,这反过来又减少了ArcA-P库。出乎意料的是,fnr基因(编码参与厌氧代谢的全局调节因子)中的突变也减轻了厌氧抑制作用。arcB或arcA中的突变对fnr突变具有上位性。此外,由于这种缓解作用在生长培养基中会被丙酮酸抵消,Fnr似乎会影响ArcB刺激因素的形成。Fnr也有可能间接影响arcA调节子的其他一些成员,例如,cyoABCDE(编码细胞色素o复合体)、cydAB(编码细胞色素d复合体)和sodA(编码锰依赖性超氧化物歧化酶)。