Krapp A R, Carrillo N
Departamento de Ciencias Biológicas, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Argentina.
Arch Biochem Biophys. 1995 Feb 20;317(1):215-21. doi: 10.1006/abbi.1995.1156.
Escherichia coli cells carrying the mvrA mutation are unable to grow aerobically in the presence of the radical propagator methyl viologen (MV). Resistance against MV toxicity could be restored by the introduction of cloned DNA sequences encoding pea chloroplast ferredoxin-NADP+ reductase (FNR), a member of a class of flavoenzymes involved in redox pathways in bacteria, plants and animals. Complementation was strictly dependent on the accumulation of a functional transgenic FNR, since mutated reductases showing decreased enzymatic activities only partially rescued the MV-resistant phenotype. These results support recent observations suggesting that the E. coli mvrA gene encodes a ferredoxin (flavodoxin)-NADP+ reductase (V. Bianchi et al. (1993) J. Bacteriol. 175, 1590-1595). The mvrA mutant cells showed a moderate decrease in the flavodoxin-dependent activation of enzymes essential for anaerobic growth of E. coli. This effect is prevented by expression of a functional pea FNR in the mutant cells.
携带mvrA突变的大肠杆菌细胞在自由基引发剂甲基紫精（MV）存在的情况下无法进行有氧生长。通过引入编码豌豆叶绿体铁氧还蛋白-NADP⁺还原酶（FNR）的克隆DNA序列，可以恢复对MV毒性的抗性，FNR是一类参与细菌、植物和动物氧化还原途径的黄素酶成员。互补作用严格依赖于功能性转基因FNR的积累，因为显示酶活性降低的突变还原酶只能部分挽救MV抗性表型。这些结果支持了最近的观察结果，即大肠杆菌mvrA基因编码一种铁氧还蛋白（黄素氧还蛋白）-NADP⁺还原酶（V. Bianchi等人（1993年）《细菌学杂志》175卷，第1590 - 1595页）。mvrA突变细胞在大肠杆菌厌氧生长所必需的酶的黄素氧还蛋白依赖性激活方面表现出适度下降。在突变细胞中表达功能性豌豆FNR可防止这种效应。
