SUMMARY: The genetic investigation of forty-three phenotypically classified cysteineless mutants of by means of transduction suggests that in forty-one of the mutants, strains of similar phenotype result from mutations occurring at a series of sites which form a closely linked group, presumably situated within a single gene locus. Five such loci have been identified. Only two of these five presumptive loci are linked, and within these linked loci an unusually high proportion of mutations to auxotrophy appear to result from a chromosomal deficiency. Another locus which is linked to an array of loci controlling tryptophan biosynthesis shows biochemical heterogeneity within the locus.


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