230 



ROBERT L. SINSHEIMER 



degradation appears to be more rapid than with the T-even phages and 

 a marked decline in total cellular DNA is observed (Fig. 6). Fifty per 

 cent of the host DNA is degraded in the first 4 minutes, and 70-80 % 

 by 10 minutes. During this time the T5 DNA is not degraded, as evi- 

 denced by retention of an adenine-C 14 label for at least 20 minutes after 

 infection. Curiously, this breakdown of host DNA does not seem to re- 

 quire the injection of the phage DNA as it proceeds in the presence of 

 external citrate which blocks injection, and it is well under way within 

 4 minutes, while injection is not normally completed until 10 minutes 

 after infection. 



This degradation of the host DNA appears to require prior protein syn- 

 thesis. It is inhibited or completely blocked by the addition at the time 

 of infection of chloramphenicol, or tetracycline, or amino acid analogs, 

 or by withholding the essential metabolite to infected auxotrophic coli 

 strains requiring proline, adenine, or uracil. This requirement for protein 

 synthesis can be rapidly satisfied, as a delay in the addition of chloram- 

 phenicol of only 1 minute after infection permits extensive, if retarded 

 DNA degradation. 



Following degradation of the host DNA, a rapid synthesis of presumably 

 viral DNA is initiated at about 10 minutes after infection which results 

 in a fivefold increase in total cellular DNA by the time of lysis. At its 

 most rapid period the rate of DNA synthesis is 5 times that of the bac- 

 terial host. 



o Control 



600 



o 500 



< 400 - 



300 



200 



100 



40 60 



MINUTES 

 Fig. 6. The effect of the addition of chloramphenicol at various times (indicated 

 on the right) during infection with bacteriophage T5 upon DNA synthesis in the 

 phage-bacterium complex. [From L. V. Crawford, Virology 7 , 359 (1959).] 



