Complementation in balanced heterokaryons and heterozygous diploids of Aspergillus nidulans

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Abstract
1. Two total and five leaky sorbitol mutants isolated in Aspergillus nidulans by defective growth on the sugar are all recessive. The mutants are closely linked, they appear to represent three linked genes spanned by a deletion.2. Mutants which complement in heterozygous diploids do not complement in balanced heterokaryons. Failure to complement is a property of the mutants and not the result of a nutritional interaction or an unfavourable nuclear ratio in the heterokaryons.3. Sorbitol is oxidized by an inducible enzyme system in the wild-type. There are at least two enzymes concerned in the oxidative assimilation of sorbitol, an initial oxidative enzyme, which is defective in the leaky mutants, and a later enzyme defective in the total mutants. There may also be a second non-oxidative pathway for sorbitol metabolism.4. In diploids complementary pairs of mutants oxidized sorbitol at 75% the rate of the wild-type but non-complementary mutants did not oxidize the sugar. In balanced heterokaryons none of the pairs of mutants oxidized the substrate. It is concluded that failure of inter-genic complementation in the heterokaryons is the result of a failure of either enzyme formation or enzyme function. Models to account for differences in enzyme formation in heterokaryons and diploids are suggested.