GENETIC CONTROL OF CELL INTEGRATION 



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inducer, and continues for some time, eventually stopping unless inducer 

 is added. With the reciprocal cross (cross 2), however, no j3-galactosi- 

 dase whatsoever is formed in the absence of inducer. These results have 

 been interpreted by Pardee, Jacob, and Monod, who did the experiments, 

 to demonstrate that the i" factor produces nothing which interferes with 

 /3-gaIactosidase formation, so that as soon as the z"^ factor enters, enzyme 

 formation may begin. Since the z"*" and i'^ factors are closely linked, and 

 virtually enter together, it must also be postulated that z"*" acts much 

 faster than does i"*". They propose that the i"*" factor produces a re- 

 pressor of /3-galactosidase, and that the reason why i"*" strains are in- 

 ducible, is that inducer must be added to antagonize the preformed 

 repressor. In the z^ i"^ cells of cross 2, which are the F~ receptors, the 

 cytoplasm is postulated to contain this repressor, and, consequently, the 

 entrance of the z~ i~ genes is of no avail. The results also show that 

 i"*" is dominant to i" . 



FIGURE 11.16. Formation of ^-galactosidase in E. coli zygotes from the cross 

 Hfrz^ i^ X F~ z' i~. Enzyme formation begins as soon as the z^/^ region en- 

 ters the F~ cell, and persists for some time in the absence of inducer. Phage 76 and 

 streptomycin are added to kill the Hfr cells (which are 76s str-s). In the reciprocal 

 cross, no enzyme is formed in the absence of inducer (after Pardee, Jacob, and 

 Monod, 1959, J. Molec, Biology, 1:165). 



