xviii Introduction 



the same bacterial cell. This is the phenomenon of multiplicity reactivation, 

 discovered by Luria in 1947 (106) and investigated in some detail by Lm-ia 

 and Dulbecco (112), whose paper is included in this collection. The quan- 

 titative results presented here seemed to bear out Luria's proposal that each 

 inactivating UV lesion represents a lethal mutation in one of a certain number 

 of genetic subunits of the phage and that multiplicity reactivation ensues from 

 the genetic exchange of still undamaged units between the two irradiated 

 parent viruses. In order to explain the very high frequency of reactivation, 

 furthermore, it was assumed that phage growth occurs by the independent 

 reproduction of each subunit, followed by reassembly of the units into com- 

 plete phages. When Dulbecco (50) subsequently continued his multiplicity 

 reactivation studies, he found that the results observed at very high UV doses 

 are no longer compatible with the notion of independently multiplying sub- 

 units. In any case, studies on genetic recombination in phage had in the mean- 

 time indicated that the genetic material of the phage does not multiply in the 

 form of independent subunits (150). More recently, however, modifications 

 of the original hypothesis of multiplicity reactivation have been proposel by 

 Baricelli ( 10 ) and by Harm ( 62 ) , which still retain that most essential element 

 of Luria's hypothesis that reactivation proceeds by a mechanism of genetic 

 exchange of undamaged parts and which lead to quantitative formulations in 

 satisfactory agreement with the observed data. 



Another radiobiological method of inactivation bacterial viruses was dis- 

 covered by Hershey, Kamen, Kennedy, and Gest (76), who showed that 

 highly P^ --labeled bacteriophages lose their infectivity upon decay of radio- 

 phosphorus atoms. From the kinetics and efficiency of this inactivation process, 

 it could be inferred that the cause of death is the transmutation of phosphorus 

 into sulfur atoms in the polynucleotide chains of the viral DNA, or the highly 

 energetic nuclear recoil associated with this event. These studies were 

 extended by Stent and Fuerst ( 141 ) , whose paper appears in this collection. 

 They found that, although the efficiency of killing of one lethal hit per ten 

 P^- disintegrations first observed by Hershey and his co-workers also obtains 

 in a variety of different bacteriophage strains, the fraction of disintegrations 

 that are lethal depends on the temperature at which decay is allowed to 

 proceed. A mechanism for the decay inactivation process of the virus was 

 suggested on the basis of these findings. It was proposed that the high pro- 

 portion of nonlethal decays reflects the possibility that the physiological func- 

 tion of the double-stranded DNA molecule is preserved even after radioactive 

 decay has interrupted only one of its polynucleotide strands. The lethal decays, 

 in contrast, are thought to be those that result by chance in a complete cut 

 of both strands of the DNA double helix. The decay of incorporated P^- atoms 

 has proven a very useful tool for the study of the structure, physiology, and 

 genetics of bacterial viruses and bacteria. (Review: 142.) 



In the hope of measuring the extent to which the infecting parental virus 

 has multiplied within the host cell during the eclipse period before the appear- 



