520 KAISER AND JACOB 



genetic material of a phage associated witii a particular locus of the 

 bacterial chromosome. If then the Ci region of the phage were responsible 

 for the association, the three functions — lysogenization, localization, 

 and immunity — would all depend on the Ci region. In the following 

 discussion this idea will be explored in more detail. 



The simplest way to explain how the Ci controls the specificity of 

 prophage localization would seem to be that the prophage is attached to 

 the bacterial chromosome by its Ci region. The Ci region of X would attach 

 to the X locus in K12, the Ci region of 434 to the 434 locus. A slight 

 structural change in a Ci region might prevent attachment. Thus it would 

 be easy to see how a mutation in the Ci region could prevent 

 lysogenization. 



The role of the Ci region in immunity may be summarized in the fol- 

 lowing way. The fact that X but not 434hy can reproduce in K12(434) 

 shows that immunity is directed against the Ci region of a superinfecting 

 phage. The fact that X but not 434 can reproduce in K12(434hy) shows 

 that immunity is governed by the Ci region of the prophage. Thus the 

 prophage controls the inhibition of vegetative multiplication of superin- 

 fecting particles possessing an homologous Ci region. This may be ex- 

 plained by two types of hypothesis. Either immunity operates in the 

 bacterium at the chromosomal level and is due to some steric hindrance, 

 or immunity is a cytoplasmic expression of a genetic function of the pro- 

 phage. This could be either the production of an "immunity substance" 

 (Bertani, 1955) by the prophage-bacterial chromosome system or the 

 inhibition by the prophage of the production by the bacterium of a 

 substance necessary for the multiplication of homologous particles. No 

 decision between these hypotheses can be reached until further attempts 

 have been made to dissociate the genetic control of lysogenization, 

 specificity of prophage location, and specificity of immunity. 



The Ci region of the prophage also controls the ability of T4rii to 

 multiply on lysogenic K12. The mechanism of this effect remains un- 

 known but the same hypothesis as those proposed for immunity may be 

 considered (Lederberg, 1957). 



ACKNOWLEDGMENTS 



We want to thank Dr. Andre Lwoff in whose laboratory at the Institut Pasteur 

 much of this work was carried out. During this time the senior author was a fellow 

 in cancer research of the American Cancer Society. 



364 



