192 ROBERT L. SINSHEIMER 



cause inactivation — failure to initiate a successful infection — of the particle 

 affected when studied in single infection. Such particles can, however, still 

 adsorb to susceptible bacteria and can inject their DNA. Unless very 

 heavily damaged, their infection results in the death of the bacterium. 44 



These inactivated particles can be "reactivated," in whole or in part, 

 in three distinct ways: photoreactivation, multiplicity reactivation, and 

 cross-reactivation. 



It has been observed that when bacteria infected with ultraviolet inactivated 

 particles are irradiated with strong near ultraviolet or blue light (3200-4500 A.) 37 ' 38 

 a significant fraction of the complexes are reactivated and go on to produce normal 

 viable phage progeny. The evidence available 39 ' 48 suggests that a certain fraction 

 (which is variable among different types of phage) of the ultraviolet lesions are 

 directly reparable by an unknown biochemical process initiated by the reactivating 

 light 46 (see Chapter 30) . 



If the infection with ultraviolet inactivated phages is made at a multiplicity of 

 phage per bacterium of two or more, instead of a single infection, the infection is 

 successful in many more cells than would be expected from occasional infection with 

 a survivor. This phenomenon 47 - 49 is known as multiplicity reactivation (MR). If the 

 ultraviolet inactivated phage is composed of a mixture of strains with known genetic 

 differences, the progeny are observed to contain a high proportion of genetic re- 

 combinants. 42 



Multiplicity reactivation is explained by the hypothesis that the ultraviolet 

 lesions distributed at random will in general inactivate different sites in the indi- 

 vidual particles infecting a particular cell. Then by recombination during or after 

 multiplication — very likely during the first replicative act 42 — an undamaged phage 

 genome can be assembled. If all particles have lesions of a type which prevent replica- 

 tion, it may be that replication can only be initiated through a recombinational event. 

 It is believed that recombination cannot take place before replication, but that it 

 can be very efficient in that even if the same functional genetic unit (cistron) were 

 damaged on, say, all infecting particles, an intact functional unit could be reas- 

 sembled unless the two lesions were by chance at nearly identical sites within the 

 cistron. However, it seems likely that certain cistrons must function before replica- 

 tion. Lesions to all of the representatives of a given cistron would then be fatal as 

 such damage could not be repaired by a recombinational event at replication. 



The third type of reactivation — cross-reactivation — is partial. If ultraviolet ir- 

 radiated phage at low multiplicity infect a cell simultaneously with unirradiated 

 phage particles of a different genotype, genetic traits of the ultraviolet treated phage 

 appear widely among the progeny. These are believed to be the results of recombina- 

 tions, during replication of the normal phage, with the genome of the irradiated 

 phage, resulting in "rescue" of the genetic traits of the latter. 60 



44 S. E. Luria and M. Delbriick, Arch. Biochem. 1, 207 (1942). 



45 E. S. Lennox, S. E. Luria, and S. Benzer, Biochim. et Biophys. Acta 15, 471 (1954). 



46 C. S. Rupert, S. H. Goodgal, and R. M. Herriott, J. Gen. Physiol. 41, 451 (1958). 



47 S. E. Luria, Proc. Natl. Acad. Set. U. S. 33, 253 (1947). 



48 S. E. Luria and R. Dulbecco, Genetics 34, 93 (1949). 



49 R. Dulbecco, J. Bacteriol. 63, 199 (1952). 



60 A. H. Doermann, M. Chase, and F. W. Stahl, J. Cellular Comp. Phijsiol. 45, Suppl. 

 2, 51 (1955). 



