280 Action of the Genetic Material 



mentioned method how far this synthesis has gone or where it has 

 been interrupted in the deficient mutant. In many cases the actual 

 seriation was revealed only by these experiments. The general result 

 in testing many mutants was that each interrupted synthesis at one 

 point only, between C and D, or between A and B, and so on. Since 

 all synthetic steps of such kind are controlled (catalyzed) by specific 

 enzymes, it may be concluded that in the deficient strains the mutant 

 gene was unable to produce the specific enzyme catalyzing the step 

 A — > B, and so on. From this the conclusion was drawn that the 

 normal gene produces this enzyme in a one-one relation, a conclusion 

 which we have discussed as a not cogent extrapolation. 



This one-one relation was interpreted to mean the following. The 

 genes (following the template idea; see above) are permanent models 

 in the image of which enzyme proteins are constructed. (This is, in 

 my opinion, an unavoidable theory of the production of the primary 

 gene products as duplicates of genie material. Beadle's concept is 

 more narrow than ours because his idea is linked with the classic 

 concept of the gene. Our concept permits these primary gene products 

 to be of many different molecular compositions according to the part 

 of a pattern which is copied. However, for the general discussion this 

 is irrelevant so long as we understand that one gene and its replica, 

 the enzyme, is only one of the possibilities.) As each synthetic step 

 requires a specific enzyme, and as each synthetic step is supposed to 

 be controlled by one gene, each specific enzyme has its master pattern 

 in one gene. In the absence of or deficient function of the gene 

 (mutation), the specific enzyme cannot be formed. 



For our subsequent discussion it might be useful to state here 

 in advance the specific progress made by this theory as well as its 

 general trend. We mentioned previously the early authors who had 

 assumed that the gene acts as an autocatalyst (the school of J. Loeb, 

 especially A. R. Moore, 1910, 1912; further, Hagedoorn, 1911; Troland, 

 1917; and Goldschmidt, 1916a, 1920a). Since, at that time, the 

 chemistry of the enzymes was practically non-existent, a specific idea 

 linking genes and products could not be proposed. Therefore, the 

 kinetics rather than the material of the gene-controlled reactions were 

 moved to the foreground in my theory of genie action through rates 

 of reaction (Goldschmidt, 1916a, 1916c, 1920a). Beadle's work shifted 

 the center of interest to the protein specificities, proposed an actual 

 chemical nature of the primary gene products, thus studied a step 

 prior to those with which our early work was concerned, and, of 

 course, introduced specific biochemical notions for our very generalized 



