220 A. GAREX AND L. M. KOZLOFF 



was quite different. In crosses between h mutants, no h^ recombinants could 

 be detected. Since all of the h mutants appear to be genetically identical by 

 this sensitive test, a mutation to h in any h^ strain must restore the original 

 h genotype. In summary: the capacity of an h strain of T2 to attach to B/2 

 cells can be lost by any one of several different h^ mutations occurring within 

 a hmited region of the chromosome, and this capacity can be regained only 

 by a reverse mutation which restores the original h genotype. 



Accordingly, the host-range region of the chromosome of an h strain 

 probably determines a specific configuration at the tip of the phage tail 

 which is required for attachment to B/2. The modifications of this tail con- 

 figuration introduced by /*+ mutations cause the loss of all affinity for B/2. 

 It should be noted that the /i+ mutants are selected for their ability to infect 

 B cells as well as for their inability to infect B/2 ceUs. This means that the 

 A"*" mutations must modify the phage tail in a way that specifically blocks 

 attachment to B/2 but not to B. There are likely to occur other mutations 

 which also block attachment to B and therefore go undetected. With some 

 of the A+ mutants the rate of attachment to B is m fact decreased, but 

 not sufficiently to prevent plaque formation (Streisinger and Franklin, 

 1956). 



The /i+ mutants of T2 may differ from the h parent in their susceptibility 

 to inactivation by heating (Hershey and Davidson, 1951; Streisinger and 

 Franklin, 1956); the heat sensitivity may be greater or lesser than it is for 

 the parental h strain. Heat-inactivated particles cannot attach to sensitive 

 cells, probably because the structure of the tail tip has been altered through 

 protein denaturation. The heat inactivation properties show that different 

 h^ mutations modify the tail structure in different ways, although all of the 

 mutations bring about the loss of affinity for B/2. 



The specific effect of A+ mutations on attachment to resistant cells can be 

 accounted for formally in either of two ways. One way is to assume that there 

 are two separate kinds of attachment sites on the phage, one for attaching 

 to sensitive cells and the other to resistant cells (perhaps located on different 

 tail fibers), and that each site is under independent genetic control. The /*+ 

 mutations would then modify only sites of the second kind. The other way 

 is to assume that there is only one kind of site on the phage for attaching 

 both to sensitive and to resistant cells, and that certain modifications of this 

 site caused by h^ mutations selectively destroy the capacity to attach to 

 resistant cells. (There also are two corresponding ways to account for the 

 difference between phage-sensitive cells and phage-resistant cell mutants; 

 by postulating either two kinds of cellular sites under independent genetic 

 control, one for binding h particles and the other for binding It^ , or a single 

 kind of site susceptible to mutational modifications that selectively destroy 

 its affinity to bind h^ particles.) 



