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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.
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