228 ROBERT L. SINSHEIMER 



decay of P 32 in parental DNA, they are 20 times less sensitive to ultraviolet radiation 

 than is free phage, and the sensitivity to X-radiation has assumed the form of a 

 multiple target curve, of multiplicity about 10, and with an asymptotic slope similar 

 to that of free phage. 6 



With phage T2 a decline in sensitivity of the complex to ultraviolet inactivation, 

 of a factor of two, is observed during the first 4 or 5 minutes. No similar decline is 

 observed in sensitivity to X-radiation or parental P 32 decay. Following this period 

 the changes observed in the 5 to 15 minute period of infection are similar to those ob- 

 served with T4. If the ultraviolet inactivation of the T2 complexes is measured after 

 maximal photoreactivation, however, it is found that there is no change in sensitivity 

 during the first 4 to 5 minutes. Symonds has interpreted these results to mean that 

 phage T2, which is as a free phage twice as sensitive to ultraviolet radiation as T4, is 

 subject to a specifically functional and photoreactivable type of damage to critical 

 cistrons which must function before replication. 40 As these cistrons are brought 

 into function during the first 4 minutes, sensitivity to this damage is lost and the 

 over-all sensitivity of the complex declines. Similar damage presumably occurs to 

 T4 complexes but is rapidly repaired by the action of the u + locus described by 

 Streisinger. 141 • 142 



Two general patterns of explanation have been developed to account 

 for the decline in sensitivity of the complexes to these various modes of 

 inactivation. 6 One hypothesis relates this decreased sensitivity to com- 

 pletion of certain necessary phage functions such as enzyme production 

 and to the production of multiple copies of the phage DNA, thus, per- 

 mitting the repair of damages by such processes as multiplicity reactiva- 

 tion. The other hypothesis postulates a transfer of the essential infor- 

 mation from DNA to an inherently less ultraviolet-sensitive and P 32 

 decay-sensitive structure such as a protein or conceivably a ribonucleo- 

 protein. 



The most cogent argument in favor of the latter hypothesis appears 

 to be the remarkable observation by Stent, 6 ' 17 ° that even when he used 

 parental phage heavily labeled with P 32 , with bacteria equally heavily la- 

 beled by growth in P 32 medium, and allowed the infection to take place 

 in heavily P 32 -labeled medium, the complexes still became insensitive to 

 P 32 decay during the later stages of the eclipse period. Under these condi- 

 tions all daughter replicas of the parental phage DNA should be heavily 

 P 32 -labeled and therefore also sensitive to P 32 decay. The possibility of 

 reconstitution of an active phage after P 32 decay by multiplicity reacti- 

 vation, appears to have been partially excluded by the observation that 

 multiplicity reactivation is not observed after P 32 decay in labeled phage 

 in multiply phage infected bacteria, whether the decay is allowed to take 

 place before or after injection. It is still conceivable that multiplicity 

 reactivation may be possible if the P 32 decay takes place after certain essen- 

 tial functions have been performed by the intact DNA in the early min- 

 utes of infection. Stent's suggestion that the essential information is trans- 



