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Summary: A mutant of Aspergillus flavus accumulating norsolorinic acid and approximately 50% less aflatoxin than the parent strain was recovered after treatment of conidia with N-methyl-N'-nitro-N-nitrosoguanidine. The gene nor controlling this mutant phenotype was recessive and linked to afl-1 and leu on linkage group VII. Diploids homozygous for nor were similar to haploids in norsolorinic acid accumulation. The analysis of recombinant diploids and haploids showed that afl-1 and nor were both distal to leu on the same chromosome arm.

A dominant mutant of Aspergillus flavus impaired in aflatoxin production, designated afl-1 and linked to leu in linkage group VII, was recovered after treatment of conidia with N-methyl-N'-nitro-N-nitrosoguanidine. Mutant afl-1 failed to complement other non-allelic aflatoxin mutants in diploids and also restricted aflatoxin accumulation when paired with toxigenic strains in diploids. No detectable effect of afl-1 was demonstrated in heterokaryons. This gene locus is apparently not involved in the extracellular degradation of aflatoxin.