The carnitine-responsive mutant yeast 26014, when grown on medium supplemented with carnitine, contained acetyl- and propionylcarnitines, consistent with the presence of carnitine acetyltransferase, which catalyses the reaction carnitine + acyl-CoA → acylcarnitine + CoA. Two hypotheses for the metabolic function of carnitine were tested. (1) That by reacting with acyl-CoA and releasing CoA, carnitine decreases the requirement for CoA. The effect of carnitine on the growth of the organism was measured in medium containing limiting amounts of pantothenate, which is a component of CoA. Carnitine did not increase the cell yield, suggesting that it did not exert a pantothenate-sparing effect. (2) That carnitine facilitates utilization of short-chain fatty acids. Carnitine reversed the growth inhibition which occurred when acetate was present in the medium, and also increased the respiration rate when acetate was the substrate, results consistent with the hypothesis that the carnitine acetyltransferase system was the limiting factor in transport of acetyl groups into mitochondria of 26014.

The properties of the carnitine-responsive strain were compared with those of the wild-type, 22987. Growth rate of the wild-type was rapid and was not stimulated by carnitine, nor was it inhibited by acetate in the growth medium. Acetate increased the respiration rate of the wild-type to the same extent in the presence or absence of carnitine. It is postulated that the mutant lacks a mechanism for handling acetate which is present in the wild-type, and that addition of carnitine to the medium enables the carnitine acetyltransferase system of the mutant to increase the rate of transport of acetyl groups into the mitochondria.


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