Ascenzi J M, Vestal J R
J Bacteriol. 1979 Jan;137(1):384-90. doi: 10.1128/jb.137.1.384-390.1979.
When Mycobacterium convolutum R22 was grown on the n-alkanes C13 through C16, the predominant fatty acids were of the same chain length as the growth substrate. Cells grown on C13 through C16 n-alkanes incorporated between 15 and 85 pmol of acetate per microgram of lipid into the fatty acids, whereas acetate- or propane-grown cells incorporated 280 and 255 pmol of acetate per microgram of lipid, respectively. In vivo experiments demonstrated that hexadecane, hexadecanoic acid, and hexadecanoylcoenzyme A (CoA) all inhibited de novo fatty acid synthesis. Hexadecanoyl-CoA was the most potent inhibitor. Hexadecane and hexadecanoic acid inhibited acetyl-CoA carboxylase by up to 37 and 39%, respectively, at 1 mM. Hexadecanoyl-CoA inhibited the enzyme activity by 65% at 50 micrometer. Cells that were grown on C14 through C16 n-alkanes had about 25 times less acetyl-CoA carboxylase activity than did cells grown on acetate or propane, suggesting repressed levels of the enzyme. Hexadecane- or pentadecane-grown cells were found to have 5 to 10 times more intracellular free fatty acid than cells grown on acetate, propane, or ethane.
当卷曲分枝杆菌R22在C13至C16的正构烷烃上生长时,主要脂肪酸的链长与生长底物相同。在C13至C16正构烷烃上生长的细胞,每微克脂质中脂肪酸掺入的乙酸盐为15至85皮摩尔,而在乙酸盐或丙烷上生长的细胞,每微克脂质中分别掺入280和255皮摩尔乙酸盐。体内实验表明,十六烷、十六酸和十六酰辅酶A(CoA)均抑制脂肪酸的从头合成。十六酰辅酶A是最有效的抑制剂。在1 mM浓度下,十六烷和十六酸分别使乙酰辅酶A羧化酶的活性抑制高达37%和39%。在50微摩尔浓度下,十六酰辅酶A使该酶活性抑制65%。在C14至C16正构烷烃上生长的细胞,其乙酰辅酶A羧化酶活性比在乙酸盐或丙烷上生长的细胞低约25倍,这表明该酶的水平受到抑制。发现十六烷或十五烷上生长的细胞,其细胞内游离脂肪酸比在乙酸盐、丙烷或乙烷上生长的细胞多5至10倍。