Defective transamination, a mechanism for resistance to ketomycin in Escherichia coli

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.