260 Action of the Genetic Material 



action upon the rate; the mutant, by an indirect action through the 

 change of a causative agent for the control of the rates. I think that 

 this point is important for any discussion of the relation of mutant and 

 phenocopy, though it has been largely overlooked. (Hadorn, 1948, 

 emphasized somewhat similar ideas.) 



This deduction becomes important when we think, for example, 

 of Landauer's ( 1945-1953 ) recent work on phenocopies in the chick, 

 about which we shall hear more below. He finds that he can induce 

 certain phenocopies by treatment of embryos with insulin. In further 

 experiments he found that the phenocopic action can be suppressed 

 by nicotinamide and riboflavin, but that the same treatment does not 

 inhibit the mutant effect. This makes him skeptical toward the as- 

 sumption that the mutant produces its effect by the same processes as 

 the phenocopy. The above-mentioned considerations show where 

 the error of such conclusions lies: the treatment in the case of the 

 phenocopy directly affects the process which has been changed by 

 the insulin treatment, restoring it more or less to normal and thus 

 preventing its effect upon the growth rate. The treatment of the 

 mutant with riboflavin may be effective or not effective (the latter 

 being the case) according to the nature of the primary process, which 

 may or may not be the same as that after insulin treatment. If it is 

 not the same, riboflavin remains ineffective, though mutant and 

 phenocopy act by influencing growth rates, whatever the primary 

 cause for this change. Thus the conclusion is correct that both mutant 

 and phenocopy produce the same phenotype because both interfere 

 with the same kinetic processes of development, though there is no 

 reason to expect that this interference works by the same means. 

 Theoretically, it would be possible to find many more types of inter- 

 ference than those found in the experiments, for example, direct 

 interference with the kinetics of growth by temperature action. Thus 

 Landauer's beautiful work does not at all change our concept of the 

 relation between mutant and phenocopy. It is fair to state that 

 Landauer ( 1952fl ) realizes this situation when he says, in regard to 

 the experiments preventing the phenocopic insulin action by riboflavin, 

 while riboflavin does not prevent the mutant action: "It is also pos- 

 sible, however, that such experiments cannot succeed, either because 

 the mutant genes change the events of development too early to be 

 repaired by supplementation or because they affect metabolic links 

 different from those involved in the origin of our phenocopies, or be- 

 cause of still other reasons." 



Let us return to the statement made above, that the primary 



