EADIOBIOLOGY OF BACTERIOPHAGE 



375 



this j)eriod should be marked by no change in sensitivity. Such a result is 

 found for T4 growing in E. coli B (Streisinger, 1956; Symonds and McCloy, 

 1958). The idea (invoked by Krieg (1958) to explain the high sensitivity of 

 the function of the rll cistrons) of two classes of damage, both of which 

 inactivate function, but one of which can be erased by the act of duplication, 

 might explain the slight change observed with T2 (Sjononds and McCloy 

 1958). 



1< 



> 10 



100 200 



Uy dose (sec) 



300 



Fig. 11. Survival curves for singly infected T2 complexes irradiated with ultraviolet 

 light at different times during the latent period. Each curve is marked with the time in 

 minutes following infection. The latent period for T2 is 19 mmutes long. This figure is 

 from Benzer (1952) and is reproduced by permission of the Williams and Wilkins 

 Company. 



The rapid change in sensitivity after 6 minutes marks the formation of 

 the first new vegetative particles and, thereby, the opportunity for multi- 

 plicity reactivation. Thereafter, since all predupHcational functions have 

 been performed, multiplicity reactivation occurs with essentially 100 % 

 efficiency rendering the complexes highly resistant. 



The residual sensitivity at the time of maximal resistance may reflect: 

 (1) a slight dependence of multipKcity reactivation on nonvulnerable parts 

 of the genome (Barricelli, 1956); (2) the dependence of the complex upon a 

 few phage-producing centers which have a sHght but significant sensitivity 

 (Epstein, H. T., 1956); or (3) the loss of complexes due to lysis of the cells 

 before the completion of the reactivation (Symonds, 1957). 



The interpretation given here to the Luria-Latarjet experiment with 

 T-even phage finds support in four observations. (1) DNA synthesis begins 



