Regulation of fatty acid biosynthesis by hydrocarbon substrates in Mycobacterium convolutum.
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.
D000085:Acetates / Q000378:metabolism; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D000214:Acyl Coenzyme A / Q000494:pharmacology; D000473:Alkanes / Q000378:metabolism* / Q000494:pharmacology; D005227:Fatty Acids / Q000096:biosynthesis*; D005230:Fatty Acids, Nonesterified / Q000096:biosynthesis*; D009161:Mycobacterium / Q000378:metabolism*; D010168:Palmitates / Q000494:pharmacology; D011407:Propane / Q000378:metabolism
D000085:Acetates; D000214:Acyl Coenzyme A; D000473:Alkanes; D005227:Fatty Acids; D005230:Fatty Acids, Nonesterified; D010168:Palmitates; D000103:Acetyl-CoA Carboxylase; D011407:Propane