Abstract
SOME phage-resistant mutants of Escherichia coli are resistant to some colicines, and vice versa1,2. Among mutants selected for resistance to colicine B four different classes result from mutation near the try (tryptophan-requirement) locus: (1) resistant to colicines B and I; (2) resistant to colicines B, I and V and to phage T1; (3) like (2), but tryptophan-exacting, responding also to indole; (4) like (2), but tryptophan-exacting, not responding to indole. The phenotypes of these four classes and genetic analysis by transduction using phage P1 and several trypto-phan-exacting mutants3 of E. coli K12 suggest that mutants of classes (2), (3) and (4) arise by multi-site mutations (presumably deletions) of variable extent (Fig. 1), in class (3) involving the try 2 locus, with resulting inability to convert indole glycerophosphate to indole, and in class (4) involving both try 2 and try 1, with resulting inability to convert indole glycerophosphate or indole to tryptophan. Yanofsky and Lennox3 similarly concluded that tryptophan-exacting phage-T1-resistant mutants, which include classes (3) and (4), arose by deletion.
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References
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GRATIA, J. Effect of Multi-site Mutation to Colicine Resistance on Recombination and Segregation in Escherichia coli. Nature 196, 1337–1338 (1962). https://doi.org/10.1038/1961337a0
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DOI: https://doi.org/10.1038/1961337a0
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