Repression of acetyl-coenzyme A carboxylase by unsaturated fatty acids: relationship to coenzyme repression.
It has been reported that the level of d-biotin in the growth medium of Lactobacillus plantarum regulates the synthesis of apoacetyl-coenzyme A (CoA) carboxylase; high levels cause repression, and deficient levels effect derepression. In this study, evidence has been obtained which suggests that coenzyme repression by biotin is an indirect effect; i.e., biotin regulates the synthesis of unsaturated fatty acids which are the true repressors of the acetyl-CoA carboxylase. This was observed in an experiment in which long-chain unsaturated fatty acids were added to media containing deficient, sufficient, or excess levels of d-biotin. In every case, independently of the biotin concentration for growth, the unsaturated fatty acids caused a severe repression of the carboxylase. Saturated fatty acids were without effect. The level of oleic acid required to give maximal repression was 50 mug/ml. The free fatty acids had no adverse effect on the activity of the cell-free extracts nor on the permeation of d-biotin into the cell. Saturated and unsaturated fatty acids decreased the rate of holocarboxylase formation from d-biotin and the apoacetyl-CoA carboxylase in the extracts. It is concluded that there are at least three mechanisms that control the acetyl-CoA carboxylase in this organism: (i) indirect coenzyme repression by d-biotin, (ii) repression by unsaturated fatty acids, and (iii) regulation of the activity of the holocarboxylase synthetase by both saturated and unsaturated fatty acids.
D001710:Biotin / Q000378:metabolism*; D002701:Chloramphenicol / Q000494:pharmacology; D003065:Coenzyme A; D004794:Enzyme Repression; D005227:Fatty Acids / Q000378:metabolism* / Q000494:pharmacology; D007778:Lactobacillus / Q000187:drug effects / Q000201:enzymology* / Q000254:growth & development; D008025:Ligases / Q000096:biosynthesis*
D005227:Fatty Acids; D002701:Chloramphenicol; D001710:Biotin; D008025:Ligases; D003065:Coenzyme A