Sensitivity to treatment with polyunsaturated fatty acids is a general characteristic of the ubiquinone-deficient yeast coq mutants.

The biosynthesis of ubiquinone (Q) and the functional consequences of Q-deficiency was studied in the yeast Saccharomyces cerevisiae. Lipid extracts were prepared from various respiratory deficient mutants grown in the presence of p-[U-14C]hydroxybenzoic acid. Q mutant strains harboring mutations in the coq3, coq4, coq5, coq6, coq7, or coq8 genes were unable to produce Q and accumulated an early intermediated that corresponded to 3-hexaprenyl-4-hydroxybenzoic acid. Several respiratory deficient yeast including both nuclear and mitochondrial petite mutant strains, retain the ability to produce Q. Thus, the inability to produce Q is a specific phenotype manifested in the class of mutants termed 'coq'. Previous studies described the enhanced sensitivity of the Q-deficient yeast strain containing a deletion in the COQ3 gene to the products of autoxidized polyunsaturated fatty acids (Do et al., 1996, Proceeding of the National Academy of Science USA, 93, 7534-7539). The results presented here show this to be a general phenotype resulting from Q-deficiency, as all of the coq mutant yeast strains tested exhibit hypersensitivity to polyunsaturated fatty acid treatment.