SUMMARY: Sixty-two mutants of the filamentous fungus were isolated on the basis of resistance to the antimetabolite fluoroacetate. Of these, 14 were unable to use acetate as sole carbon source (acetate non-utilizers, ) and were the subject of further genetic and biochemical analysis. These mutants fell into four complementation groups, three of which did not complement any known mutants. Mutants of complementation group 3 failed to complement , demonstrated similar phenotypic properties and proved to be closely linked (less than 2% recombination) but not allelic. Representatives of groups 2 and 4 were mapped to independent loci; the single representative of group 1 could not be mapped. The four complementation groups were therefore designated as genes to respectively. All the mutants demonstrated normal acetate-induced expression of acetyl-CoA synthetase and the unique enzymes of the glyoxylate cycle and gluconeogenesis. The nature of these mutations is therefore quite different to those reported for other fungal species. Mutant was unable to fix labelled acetate, indicating the loss of an initial transport function; partial enzyme lesions were observed for (acetyl-CoA hydrolase) and (acetate-inducible NAD-specific malate dehydrogenase).


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