300 BACTERIOPHAGES 



and has no effect on phage or bacterium. For the present this 

 example can be left among the h mutations. 



The virulent mutants of temperate phages form one category 

 of mutants with altered growth potential (Chapter XIX). The 

 mutations decrease the frequency of lysogenization, and increase 

 the frequency of lytic infection, exhibited by the phage. Viru- 

 lent mutants produce clear plaques in contrast to the turbid 

 plaques formed by the temperate parent, and are often called c 

 mutants for this reason. Examples are described by Burnet and 

 Lush (1936), Gratia (1936b), Rountree (1949a), McCloy 

 (1951), Boyd (1951), Murphy (1952, 1954), Bertani (1953b), 

 Jacob and Wollman (1954), LwofT, Kaplan, and Ritz (1954), 

 Dickinson (1954), Barksdale and Pappenheimer (1954), Zinder 

 (1955), Levine (1957), Kaiser (1957). 



A second category of mutations affecting virulence produces 

 scrong or inducing mutants of temperate phages. Such mutants 

 can overcome the immunity to superinfection exhibited by 

 lysogenic bacteria toward temperate phages closely related to 

 the carried prophage (Chapter XIX). Strong virulent mutants 

 thus form a subclass among virulent mutants, and seem to act 

 by inducing the lytic development of the carried prophage, as 

 well as initiating their own (Jacob and Wollman, 1953). Muta- 

 tions of this type thus produce an extended host range of a special 

 kind. The inducing mutant of lambda is a multiple mutant 

 (Jacob and Wollman, 1954). Other examples are mentioned 

 by Lwoff (1953) and Bertani (1953b, 1958). 



Lysogenic bacteria are also refractory to infection by certain 

 phages unrelated to the carried prophage, including phages that 

 are virulent for the corresponding nonlysogenic bacteria. The 

 well studied example is the resistance of E. coli K12 carrying 

 prophage lambda to the rll mutants of T4 (Benzer, 1955) 

 (Chapter XVIII). The phage adsorbs to and kills the bac- 

 terium, and certainly injects, as shown by mixed infection ex- 

 periments, but usually fails to multiply. The mutation /II -^ r + 

 restores the limited growth potential to normal efficiency. 

 Other examples are cited by Bertani (1953b), and in Chapter 

 XXI 



