Harrison L I, Christensen H N, Handlogten M E, Oxender D L, Quay S C
J Bacteriol. 1975 Jun;122(3):957-65. doi: 10.1128/jb.122.3.957-965.1975.
The uptake of L-4-azaleucine was examined in Escherichia coli K-12 strains to determine the systems that serve for its accumulation. L-4=Azaleucine in radio-labeled form was synthesized and resolved by the action of hog kidney N-acylamino-acid amidohydrolase (EC 3.5.1.B) on the racemic alpha-N-acetyl derivative of DL-[dimethyl-14C]4-azaleucine. L-4-Azaleucine is taken up in E. coli by energy-dependent processes that are sensitive to changes in the pH and to inhibition by leucine and the aromatic amino acids. Although a single set of kinetic parameters was obtained by kinetic experiments, other evidence indicates that transport systems for both the aromatic and the branched-chain amino acids serve for azaleucine. Azaleucine uptake in strain EO317, with a mutation leading to derepression and constitutive expression of branched-chain amino acid (LIV) transport and binding proteins, was not repressed by growth with leucine as it was in parental strain EO300. Lesions in the aromatic amino acid transport system, aroP, also led to changes in the regulation of azaleucine uptake activity when cells were grown on phenylalanine. Experiments on the specificity of azaleucine uptake and exchange experiments with leucine and phenylalanine support the hypothesis that both LIV and aroP systems transport azaleucine. The ability of external azaleucine to exchange rapidly with intracellular leucine may be an important contributor to azaleucine toxicity. We conclude from these and other studies that at least four other process may affect azaleucine sensitivity: the level of branched-chain amino acid biosynthetic enzymes; the level of leucine, isoleucine, and valine transport systems; the level of the aromatic amino acid, aroP, uptake system; and, possibly, the ability of the cell to racemize D and L amino acids. The relative importance of these processes in azaleucine sensitivity under various conditions is not known precisely.
在大肠杆菌K-12菌株中检测了L-4-氮杂亮氨酸的摄取情况,以确定负责其积累的系统。通过猪肾N-酰基氨基酸酰胺水解酶(EC 3.5.1.B)对DL-[二甲基-14C]4-氮杂亮氨酸的外消旋α-N-乙酰衍生物的作用,合成并拆分了放射性标记形式的L-4-氮杂亮氨酸。L-4-氮杂亮氨酸在大肠杆菌中通过能量依赖过程被摄取,该过程对pH变化以及亮氨酸和芳香族氨基酸的抑制敏感。尽管通过动力学实验获得了一组单一的动力学参数,但其他证据表明,芳香族和支链氨基酸的转运系统都参与了氮杂亮氨酸的转运。在菌株EO317中,由于一个突变导致支链氨基酸(LIV)转运和结合蛋白的去阻遏和组成型表达,其氮杂亮氨酸摄取不受亮氨酸生长的抑制,而亲本菌株EO300则受抑制。当细胞在苯丙氨酸上生长时,芳香族氨基酸转运系统aroP中的损伤也导致氮杂亮氨酸摄取活性调节的变化。关于氮杂亮氨酸摄取特异性的实验以及与亮氨酸和苯丙氨酸的交换实验支持了LIV和aroP系统都转运氮杂亮氨酸的假设。外部氮杂亮氨酸与细胞内亮氨酸快速交换的能力可能是氮杂亮氨酸毒性的一个重要因素。我们从这些及其他研究中得出结论,至少还有其他四个过程可能影响氮杂亮氨酸敏感性:支链氨基酸生物合成酶的水平;亮氨酸、异亮氨酸和缬氨酸转运系统的水平;芳香族氨基酸aroP摄取系统的水平;以及,可能还有细胞将D和L氨基酸消旋的能力。这些过程在各种条件下对氮杂亮氨酸敏感性的相对重要性尚不清楚。