Williams M V, Kerr T J, Lemmon R D, Tritz G J
J Bacteriol. 1980 Jul;143(1):383-8. doi: 10.1128/jb.143.1.383-388.1980.
Resistance to azaserine in Escherichia coli is the result of mutations in at least three different loci. All spontaneously arising azaserine-resistant mutants harbor a lesion in the aroP gene. However, a lesion in this gene is not solely responsible for resistance. All spontaneously arising intermediate-level azaserine-resistant mutants also harbor a lesion in a gene designated azaA, which lies near min 43 on the chromosome. High-level resistant mutants harbor lesions in the aroP and azaA genes and in a third gene designated azaB, which lies near min 69 on the chromosome. Transport studies demonstrate that mutants harboring lesions in the azaA gene are not defective in the transport of the aromatic amino acids, but that mutants which harbor lesions in the azaB gene are defective in phenylalanine transport but not in tyrosine or tryptophan transport.
大肠杆菌对重氮丝氨酸的抗性是至少三个不同基因座发生突变的结果。所有自发产生的重氮丝氨酸抗性突变体在aroP基因中都有损伤。然而,该基因中的损伤并非抗性的唯一原因。所有自发产生的中等水平重氮丝氨酸抗性突变体在一个名为azaA的基因中也有损伤,该基因位于染色体上43分钟处附近。高水平抗性突变体在aroP和azaA基因以及第三个名为azaB的基因中都有损伤,azaB基因位于染色体上69分钟处附近。转运研究表明,在azaA基因中有损伤的突变体在芳香族氨基酸的转运方面没有缺陷,但在azaB基因中有损伤的突变体在苯丙氨酸转运方面有缺陷,而在酪氨酸或色氨酸转运方面没有缺陷。