Defective transamination, a mechanism for resistance to ketomycin in Escherichia coli.
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.
D000900:Anti-Bacterial Agents / Q000378:metabolism*; D003510:Cyclohexanes / Q000378:metabolism; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects* / Q000201:enzymology; D006038:Glyoxylates / Q000378:metabolism; D007532:Isoleucine / Q000378:metabolism; D009154:Mutation; D000637:Transaminases / Q000378:metabolism
D000900:Anti-Bacterial Agents; D003510:Cyclohexanes; D006038:Glyoxylates; D007532:Isoleucine; C008231:ketomycin; D000637:Transaminases