MUTATIONS OF BACTERIAL VIRUSES 95 



is not complete is shown by the fact that the mutant viruses are adsorbed by 

 the mutant bacteria more slowly than by the normal bacteria. One may say 

 that the affinity of the mutant viruses for the mutant bacterial strains is 

 poorer than for strain B. 



Strain B7 is sensitive to virus a and to virus 7'. Does the mutation y—*y' 

 involve the acquisition by the virus of the same structural configuration that 

 enables virus a to attack strain B7? If so, mutants from strain B7 which are re- 

 sistant to virus a should also be resistant to virus y' . It was easy to isolate from 

 B7 several a-resistant mutants, called 67a ; all of them proved perfectly sensi- 

 tive to virus y' (fig. 1). Sensitivity to viruses a and y' cannot, therefore, be due 

 to the same structural configuration. 



It was more difficult to isolate bacterial mutants stably resistant to virus 

 y' . Eventually, we obtained from strain Bon a mutant strain Ba^' that proved 

 resistant to virus 7 and to virus 7', and, surprisingly enough, sensitive to virus 

 a. The sensitivity of strain Ba^' to virus a was unexpected, since this strain 

 was a mutant from strain Ba u which was completely resistant to virus a. The 

 mutation Bai—^Baiy' , therefore, involved loss of sensitivity to viruses 7 and 

 y', but gain of sensitivity to virus a. 



It may be added that from strain Bony' a mutant Baiy'a can easily be ob- 

 tained, resistant to all three viruses a, 7, and y' (fig. 1). 



Let us now consider the situation concerning virus a . The mutation a—>ct 

 involves gain of ability to attack the a-resistant mutant Ba 2 . This ability is 

 not due to the same configuration which enables virus 7 to attack Ba 2 , as 

 proved by the fact that virus a' also attacks a mutant strain B7« 2 , resistant to 

 virus 7. Differences in the configurations of virus a' and virus y' are brought 

 out by their relations to the mutants Bya\ and Ba\y' (fig- i)- The remarkable 

 point here is that the mutation a-^a compensates for only certain mutations 

 of a-sensitive bacteria — namely, B— >Ba 2 and B7— *Bya.2, but not for the mu- 

 tations B— >Bai or B7— ►B7ai. It is worth mentioning that both strains Ba 2 and 

 B7a 2 belong to the group of "small colony" mutants that grow poorly and 

 slowly on nutrient agar, whereas Bai andB7«! are normal colony formers. This 

 is an example of a modification of the cultural, physiological properties of the 

 bacterial cells correlated with the mutational change to virus-resistance. 



The results summarized in figure 1 indicate that various bacterial mutations 

 leading to resistance to unrelated viruses are generally independent of each 

 other. For instance, the same two mutations (sub-i and sub-2) leading to re- 

 sistance to virus a (with or without resistance to virus a and change in cul- 

 tural characters) can occur either in strain B or in strain B7, in spite of the 

 fact that the latter has already undergone a mutation toward resistance to 

 virus 7. 



Figure 1 also shows the occurrence of a'-resistant strains, all of which are 

 also resistant to virus a. 



The results of this section show that some, if not all, mutational changes in 

 virus sensitivity by our bacterial strains can be compensated for by comple- 

 mentary mutations of the viruses. It is possible that in cases of bacterial mu- 

 tations for which complementary virus mutations have not been found (for ex- 



233 



