Genie Control of Development 365 



caused by different external or genetic environment (the modifiers), 

 which have been represented on the levels M, Mi, M2 (which should 

 coincide ) ; the numbers indicate the number of cell divisions that have 

 occurred at the different points. In the system Mi, division ceases 

 before six divisions are finished; and therefore the small size is almost 

 completely dominant. ( AA is characterized by stoppage after five divi- 

 sions — line M.) In M2 we have assumed that cell division proceeds 

 faster at first and later slows up. In this case, dominance of the large 

 size ( eleven divisions ) results. In this model, the variables responsible 

 for dominance are reaction velocities controlled by the loci according 

 to simple dosage relations, thresholds for morphogenetic effects, the 

 type of effect, and the numerical system of an independently deter- 

 mined process which is involved. It is obvious that the general 

 features of such a model, which permits introduction of whatever 

 variable the facts require, will fit all imaginable cases. From this we 

 may conclude that dominance teaches us, in a general way, that genie 

 action is bound up with quality and quantity of reaction products, 

 with threshold conditions of their action, and with features of the 

 kinetics of the reactions involved. We could also describe such a system 

 as the real, dynamic meaning of so-called genie balance (more cor- 

 rectly called "balance of genie actions") applied to the facts of domi- 

 nance, but applicable also to all genie actions. 



The next question is whether such a genetic system, regulating 

 dominance, may be endowed with a more specific meaning, preferably 

 a biochemical one. Wright ( 1934a ) has proposed such a variant of our 

 model. He assumes, as we also do, that there is a chain of reactions 

 between the locus and the end product and that any condition that 

 makes one link of the chain act in the heterozygote as it acts in the 

 homozygote results in dominance. Next he assumes that the gene acts 

 as a catalyst controlling the rate of production of some substance by 

 a chain of irreversible transformations, the intermediary substances 

 being in a flux equilibrium. These reactions may be monomolecular 

 and dependent on the concentration of both catalyst and substrate. 

 In this case the rate varies directly with the concentration of the 

 catalyst, and the curve expressing this will be a hyperbole. Therefore, 

 with increasing activity of the gene, its heterozygous effect should ap- 

 proach dominance. Other similar possibilities are taken into account. 

 All of which can be described as variants of our model with emphasis 

 on different phases. I point out here that the idea of different activities 

 of the gene (which in my former concept were different quantities) 

 is at the base of the hypothesis. (We shall return to this soon.) 



