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Derepression and altered feedback regulation of valine biosynthetic pathway in analogue‐resistant mutants of Streptomyces cinnamonensis resulting in 2‐ketoisovalerate excretion
Author(s) -
Pospíšil,
Vladimı́r Kopecký,
Přikrylová
Publication year - 1998
Publication title -
journal of applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.889
H-Index - 156
eISSN - 1365-2672
pISSN - 1364-5072
DOI - 10.1046/j.1365-2672.1998.00459.x
Subject(s) - derepression , valine , mutant , streptomyces , biochemistry , biology , streptomycetaceae , chemistry , actinomycetales , amino acid , genetics , gene , bacteria , psychological repression , gene expression
Excretion of 2‐ketoisovaleric acid (KIV) was demonstrated in Streptomyces cinnamonensis mutants resistant to valine analogues 2‐amino‐3‐chlorobutyrate, 2‐aminobutyrate and norleucine, respectively. The highest KIV concentrations of 170–230 mg l −1 were found in cultivation liquids of norleucine‐resistant strains. Biochemical analyses of the acetohydroxyacid synthase (AHAS), valine dehydrogenase (VDH) and branched chain amino acid aminotransferase activities revealed the deregulation of the valine‐synthesizing pathway, resulting in KIV excretion. In the 2‐amino‐3‐chlorobutyrate‐resistant strain, the activity of AHAS increased 23‐ to 31‐fold compared with the parental strain. The norleucine‐resistant mutants combined both a 10‐ to 23‐fold increase in AHAS activity and lack of efficient feedback regulation by valine. In the double 2‐amino‐3‐chlorobutyrate plus norleucine‐resistant mutant, the AHAS activity was only four to eight‐fold higher, but release of feedbackregulation was conserved. Similarly, feedback regulation was inefficient in 2‐aminobutyrate‐resistant strains, however the AHAS activity was lower than in the parental strain. A strong induction of VDH was observed in all regulatory mutants.