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W. KUNICKI-GOLDFINGER 



On the basis of this hypothesis we would postulate a double 

 specificity of streptomycin: as an inhibitor of the drug- 

 sensitive biochemical pathway, and as a mutagenic factor 

 specifically altering the genie element, governing just this 

 pathway. This mechanism is possible but rather improbable. 



To elucidate this problem some experiments were made in 

 our laboratory. We were not able to confirm these results. 

 Nevertheless, we are careful in interpretation, because the 

 conditions of our experiments were different from those of 

 Szybalski.* 



Esch. coli K 12 was used. The sensitivity of the original 

 strain to streptomycin, as assayed with the plate dilution 

 method, is shown in Table I. 



Table I 

 Sensitivity of Esch. coli K 12 to streptomycin 



Bacteria were grown in beef-heart broth, harvested after 

 20 hours of incubation, washed twice in phosphate buffer 

 (pH 7), and resuspended in the buffer to give a turbidity of 

 10^ to 10^ cells per ml. Dihydrostreptomycin (Merck) was 

 then added to bring the final concentration up to 5 \Lg. per ml. 



* In recent connnunieations on this problem Szybalski (1956) and Arndt 

 and Zinder (1956) have shown that in Szybalski's experimental conditions 

 multiplication of bacteria was possible, and was in fact going on during the 

 incubation period. The selection of spontaneous mutants was not excluded. 



