Kinetics of Phenotypic Expression 199 



agent is applied. These difficulties can be overcome to some 

 extent by subjecting bacterial populations to the action of 

 physical or chemical mutagens which not only may greatly 

 increase the total number of mutations but, at the same time, 

 will synchronize their initiation. However, the use of such 

 agents introduces other variables which may have a profound 

 effect on the sequence of events. For example, it has been 

 shown that even a low degree of irradiation with ultraviolet 

 light temporarily arrests the synthesis of deoxyribonucleic 

 acid of which the genetic material of the cell is constructed 

 (Kelner, 1953), and leads to marked aberrations in cellular 

 morphology. The extent to which mutagenic agents may 

 injure cytoplasmic as well as nuclear function is not clear, 

 but may be appreciable. 



In practice, experiments designed to determine the pheno- 

 typic lag of induced mutations, involving many different 

 types of character, have given most conflicting results. In 

 general, the delay has been found greatly to exceed that 

 required for segregation of the mutant nucleus or for the 

 cytoplasmic manifestation of its genotype (Demerec, 1946; 

 Ryan, 1954). In some systems, on the other hand, a delay of 

 less than one generation has been suggested (Ryan, 1955). 

 The work of Witkin (1956) indicates the importance of nutri- 

 tional and other factors in the environment, during the first 

 third of the first generation time following irradiation, in 

 deciding whether or not the mutational change will stabilize 

 and become expressed. 



We are thus faced with the difficulty that the nature of 

 mutation precludes the direct experimental study of its 

 kinetics unless the mutations are artificially induced, while 

 the inducing agents themselves influence the course of events 

 in such a way as to render the results of such experiments to 

 a considerable extent invalid. It is clear that the action of 

 mutagenic agents, as well as the nature of the interaction of 

 mutant genes with the metabolic processes they determine, 

 can only properly be evaluated against a background of 

 knowledge of the kinetics of segregation and phenotypic 



