Genie Control of Development 321 



material, is not considered by Waddington to be different from the 

 first, and accounted for by the same idea, which, I think, does not 

 even work for the first problem, as I tried to show. Waddington thinks 

 that it is easy to imagine how competition between genes for sub- 

 strates, which are required to a varying extent, could lead to situations 

 in which a particular complex of substrates facilitated the activity of 

 some definite constellation of genes. Thus, the generalized statement 

 that genie material becomes active when imbedded in the competent 

 substratum, which I developed ( 1927 ) , receives a special chemical 

 terminology: activation means better ability to compete for the specific 

 substrate to which the specific genie material is attuned, and the 

 competent substrate becomes a selected assembly of different quanti- 

 ties of various raw materials for synthesis. Though this view has the 

 advantage of being less generalized than mine, it still is more or less 

 indicative of our lack of factual biochemical knowledge. 



We come now to the special problems of genie activation, and 

 begin with a recent discussion by Caspari ( 1949a ) . He uses Hadorn's 

 (1945) term, "manifestation pattern," meaning that organs which are 

 not affected by a certain gene lie outside its manifestation pattern. 

 Two possibilities are given: the genie material may be active in all 

 cells at all times, and the manifestation may depend on differential 

 reactions of different cells on the metabolic changes induced by the 

 gene; or the gene may be active in some types of cells but not in 

 others. Though the discussion is not primarily applied to the problem 

 of embryonic determination, its results may apply to our present 

 problem. Caspari (1933, 1936) studied pigmentation in the flour moth, 

 which is inhibited in the mutant aa; the normal pigment is deposited 

 in the eyes, testes, and brain of the adult and the larval ommatidia 

 and hypodermis. The last character becomes visible in the embryo; 

 testis pigment, at the last larval molt; and the eye pigments, in the 

 pupal stage. The inhibition is based upon lack of kynurenine, an 

 amino acid precursor of the pigment. Almost all organs of the wild 

 type can form kynurenine and release it, if transplanted into aa 

 larvae, but some organs store it and release only a little. From such 

 facts the conclusion is drawn that all genes are active in all cells of 

 the body, though their effect — the morphological reaction pattern — 

 becomes visible only in some cells. Now Plagge (1936) showed that 

 aa testes can form pigment only if supplied with kynurenine before 

 pupation; larval ommatidia lose their ability to react at the last larval 

 molt; different types of eye cells have distinct, overlapping periods 

 in which they react to transplanted or injected AA tissue. This is 



