Defective Transamination, a Mechanism for Resistance to Ketomycin in Escherichia Coli
Overview
Authors
Affiliations
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.
Jackson J, Williams L, Umbarger H J Bacteriol. 1974; 120(3):1380-6.
PMID: 4612020 PMC: 245925. DOI: 10.1128/jb.120.3.1380-1386.1974.
Specificity of attenuation control in the ilvGMEDA operon of Escherichia coli K-12.
Chen J, Bennett D, Umbarger H J Bacteriol. 1991; 173(7):2328-40.
PMID: 1706705 PMC: 207786. DOI: 10.1128/jb.173.7.2328-2340.1991.
Mutation affecting regulation of synthesis of acetohydroxy acid synthetase in Escherichia coli K-12.
Jackson J, Henderson E J Bacteriol. 1975; 121(2):504-10.
PMID: 1089632 PMC: 245959. DOI: 10.1128/jb.121.2.504-510.1975.
Davis E, Blatt J, Henderson E, Whittaker J, Jackson J Mol Gen Genet. 1977; 156(3):239-49.
PMID: 340906 DOI: 10.1007/BF00267178.