THE INITIATION OF BACTERIOPHAGE INFECTION 219 



the nonlysogenic strain, and also contain a new surface antigen not found in 

 the nonlysogenic strain (Uetake et al., 1958). The correspondence of these 

 antigenic changes with the changes in attachment specificity (cited in the 

 preceding paragraph) suggests that the attachment sites for the phages con- 

 cerned are located on the antigens. 



The most extensive analysis of the serological and chemical effects of muta- 

 tion to resistance has been carried on mutants of Shigella sonnei and E. coli 

 resistant to phages T3, T4, and T7 (Goebel and Jesaitis, 1952; Weidel et al., 

 1954). The sensitive and resistant strains of Sh. sonnei differ serologically. A 

 purified antigen isolated from the sensitive strain reacts with the three phages, 

 but the antigen from the resistant strain is inactive. These antigens are com- 

 posed of a complex of hpocarbohydrate and protein. When the hpocarbo- 

 hydrate is isolated as protein-free hapten from the sensitive strain, it retains 

 the capacity to react with the three phages, but the corresponding haptenic 

 component from the resistant mutant does not. It is of particular interest 

 that chemical differences have been detected between the carbohydrate 

 moieties of these Hpocarbohydrate components from sensitive and resistant 

 strains of Sh. sonnei and E. coli. Further detailed studies of this kind should 

 contribute significantly to an understanding of the chemical basis of attach- 

 ment specificity. 



B. Host-Range Mutants of Phages 



By use of phage-resistant cell mutants, it usually is possible to isolate 

 phage mutants that can attach to and infect the resistant cells. This type of 

 mutant, called host range or h, can be selected for in a population of parental 

 A+ particles by plating for plaques on the resistant cells (Luria, 1945a,b). 

 The converse mutation, from h to h"^, also occurs. The /i+ particles can be 

 detected, although not selectively, by plating on a mixture of resistant and 

 sensitive cells; plaques of h'^ particles are turbid, in contrast to the plaques 

 of h particles, which are clear (Hershey and Davidson, 1951; Streisinger and 

 Franklin, 1956). 



The genetic characteristics of host-range mutations in T2 have recently 

 been analyzed in fine detail (Streisinger and Franklin, 1956). Genetic crosses 

 (see Chapter VIII, page 281) were run on two classes of mutants. One class 

 consisted of A+ mutants originating from independent mutational events in 

 an h strain. The other class consisted of h mutants originating from independ- 

 ent mutational events in several h^ strains. In pairwise crosses between /i+ 

 mutants from the first class, h recombinants were usually formed. This result 

 shows that an h^ mutation can arise at many separate locations on the chromo- 

 some of an h strain. (All the A+ mutants studied have been foimd to be 

 closely linked, that is, the mutations cluster within a limited region of the 

 phage chromosome.) The behavior of the second class of mutants, however. 



