转氨作用缺陷：大肠杆菌对酮霉素耐药的一种机制。
Defective transamination, a mechanism for resistance to ketomycin in Escherichia coli.
作者信息
Jackson J H, Umbarger H E
出版信息
Antimicrob Agents Chemother. 1973 Apr;3(4):510-6. doi: 10.1128/AAC.3.4.510.
Abstract
A spontaneous mutant of a derivative of Escherichia coli strain K-12 resistant to 50 mug of ketomycin per ml was selected. The mutant displayed a two- to threefold derepression of the isoleucine-valine biosynthetic enzymes and a reduced growth rate in minimal medium. The lesion was found to lie in the gene (ilvE) specifying transaminase B and resulted in an isoleucine limitation. The presence of exogenous isoleucine during growth in minimal medium restored normal phenotypic properties. The reduced transaminase B activity is responsible for the resistance to ketomycin. An unusual derepression of the acetohydroxy acid synthetase in response to an isoleucine limitation was noted.
摘要
从大肠杆菌K-12菌株的一个衍生物中筛选出一种自发突变体，该突变体对每毫升50微克的酮霉素具有抗性。该突变体的异亮氨酸-缬氨酸生物合成酶的阻遏解除了两到三倍，并且在基本培养基中的生长速率降低。发现损伤位于编码转氨酶B的基因（ilvE）中，并导致异亮氨酸限制。在基本培养基中生长期间添加外源异亮氨酸可恢复正常的表型特性。转氨酶B活性降低是对酮霉素产生抗性的原因。注意到在异亮氨酸限制的情况下，乙酰羟酸合成酶出现了异常的阻遏解除。
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