RADIOBIOLOGY OF BACTERIOPHAGE 381 



apparatus of the host cell. As a consequence, the ideas, if not always the 

 experiments, on their radiobiology are simpler, and form a natural unit for 

 the purposes of this review. We have exploited their exceptional behavior in 

 order to introduce the principal concepts and basic techniques of phage 

 radiobiology. Armed with these concepts, we may now look elsewhere. 



B. Survival of Infectivity 



The inactivation of all phages by ionizing radiations (direct effect) or by 

 P^^-suicide is exponential. The sensitivities to these agents are in general in 

 approximate proportion to their DNA content (Epstein, 1953; Stent and 

 Fuerst, 1955). The small phages S13 and y)X174 are anomalously sensitive 

 to suicide (Tessman et al., 1957; Tessman, personal communication). It 

 seems most likely that this is causally related to the aberrant physical 

 properties of the DNA of this phage (Sinsheimer, personal communication). 



In contrast with the simple survival curves obtained with ionizing radia- 

 tions or P32.g^^ici(je^ tlie curves found with ultraviolet light assume every 

 imaginable shape. The suggestion (Garen and Zinder, 1955) that such curves 

 often reflect a partial reactivation of the phage by the host cell seems sub- 

 stantiated for a number of systems (e.g., for Salmonella phage P22 and E. 

 coli phage T3 (Garen and Zinder, 1955), and for Tl (Garen and Zinder, 

 1955; Tessman and Ozaki, 1957). These experiments in general consist of a 

 demonstration that the survival curves for phage assayed on irradiated 

 host cells is steeper than when the assay is made on normal cells. At inter- 

 mediate doses to the host cells, the ultraviolet-survival curves of the phage 

 are two-limbed. The contribution of the high-dose limb to the survival of the 

 phage at zero dose represents the fraction of cells in which the reactivating 

 capacity remains intact. 



It is not clear whether the mechanism of reactivation of the inactive 

 phage by the host cell is by erasure or replacement, perhaps as a result of 

 genetic recombination between the phage and homologous structures in the 

 host cells. The ultraviolet-induction of mutations (see Section V, D) in many 

 such systems, however, argues for a recombinational mechanism of reactiva- 

 tion. Arguing against a recombinational mechanism are the observations 

 that with X-ray or suicide-inactivated phages cellular reactivation does not 

 appear to occur. Perhaps if these agents were to be delivered to the phage 

 after infection, host-cell reactivation might occur in analogy with the 

 increased efficiency of cross reactivation of T-even phage under these 

 conditions. 



C. Multiplicity and Cross Reactivation 



In those systems showing host-cell reactivation, multiplicity and cross 

 reactivation are relatively difficult to demonstrate. Tessman and Ozaki 



