Regulation of Citrate Efflux from Mitochondria of Oleaginous and Non‐Oleaginous Yeass by Long‐Chain Fatty Acyl‐CoA Esters

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Abstract
Citrate efflux from a wide range of yeast [Candida utilis NCYC 359; C. utilis NCYC 707; Saccharomyces cerevisiae NCYC 33; S. cerevisiae NCYC 240; Saccharomycopis lipolytica NCYC 153; Trichosporon cutaneum 40 (Iowa University); Candida curvata D (Iowa University); Rhodosporium toruloides IFO 0559; Lipomyces starkeyi CBS 6132; L. starkeyi CBS 6047] mitochondria was inhibited by long-chain fatty-acyl-CoA esters. Fatty-acyl-CoA esters with chain lengths of between 14 and 28 C were the most potent inhibitors of citrate efflux which was unaffected by the fatty acids themselves. A 50% inhibition of citrate transport was observed using palmitoyl-CoA and oleoyl-CoA at .apprx. 4-5 .mu.M when the tricarboxylate carrier was saturated with L-malate as counter-anion. The inhibition with palmitoyl-CoA and oleoyl-CoA was competitive with L-malate. The possibility that the fatty-acyl-CoA esters were exerting their effect by acting as detergent was eliminated because of the low concentrations used and appropriate comparisons being made with non-specific detergents. Although detergents inhibited citrate efflux they also released citrate by causing membrane damage. The effect of fatty-acyl-CoA esters on citrate efflux could be decreased by using higher mitochondrial protein levels and by adding bovine serum albumin. The possibility is discussed that this inhibition represents a genuine feedback inhibition which could regulate the amount of lipid being synthesized by an oleaginous yeast.

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