Defective Transamination, a Mechanism for Resistance to Ketomycin in Escherichia coli | Zendy

Julius H. Jackson | Zendy; H. E. Umbarger | Zendy

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Defective Transamination, a Mechanism for Resistance to Ketomycin in Escherichia coli

Author(s) -

Julius H. Jackson,

H. E. Umbarger

Publication year - 1973

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.3.4.510

Subject(s) - derepression , isoleucine , transamination , escherichia coli , mutant , biology , biochemistry , valine , transaminase , microbiology and biotechnology , enzyme , gene , amino acid , leucine , psychological repression , gene expression

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.

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