SYLLABUS 141 



suggests that, as in the early stages of the latent period (see 27), the 

 phage is present in the cell in a non-infective state. 



XL Lysis Inhibition 



38. Phages T2, T4, and T6 differ from their r mutants (see 8) in 

 that the r mutants produce clearing of turbid bacterial cultures at the 

 end of the latent period while in cultures infected with the wild type 

 r+ clearing is considerably delayed, sometimes for hours (Hershey, 

 1946b). This delay of clearing, which is characteristic for turbid cul- 

 tures of bacteria infected with the wild types of the even nmnbered 

 phages of the T set, is called lysis inhibition, and the letter r, charac- 

 terizing the mutants in which the delay is absent, stands for rapid lysis. 

 The difference between r and r+ has been analyzed by Doermann 

 (1948b) as follows: 



(1) Lysis inhibition is due to a second infection with phage 

 coming at least 3 minutes after the primary infection. The r+ 

 phages liberated from the first lysed bacteria are adsorbed by the 

 remaining bacteria and inhibit their lysis. 



(2) To inhibit lysis both primary and secondary infection must 

 be with r+ phage. 



(3) While one particle can inhibit lysis, the duration of the inhibi- 

 tion increases with the multiplicity of the secondary infection. 



(4) The burst size of lysis inhibited bacteria is greater than that of 

 uninhibited bacteria. 



(5) T2, T4, and T6 can cross inhibit lysis, e.g., following primary 

 infection with T2r+, a second infection by T4r+ results in lysis 

 inhibition. 



The following observations suggest that inhibition does not in- 

 volve growth of the secondarily added phage: 



(1) When a bacterium is primarily infected with T2h+r+ and 8 

 minutes later with T2hr+, lysis inhibition occurs though none of 

 the inhibited bacteria yield any T2hr+ (DeMars, personal com- 

 munication). 



(2) "Non-kilHng" X-ray inactivated T2r+ (see 21) inhibits lysis 

 as effectively as does active T2r+. This suggests that inhibition is 

 due to a stage prior to invasion and may be due to a change in the 

 bacterial surface (Watson, 1950). 



Nothing is known about the chemical mechanism of lysis inhibition. 



