THE MUTATED GENE 41 



case is to be found by applying the concept of rates of deposition 

 of pigment, which are changed by the mutant genes or stopped 

 before completion. 



Another but probably somewhat more complicated case is 

 furnished by the different hereditary abnormalities of the human 

 hand, e.g., brachyphalangy. In normal human development, 

 the second row of phalanges is formed in the third month, but its 

 development is not finished until after that of the rest of the 

 bones of the hand. In brachyphalangy, they do not appear until 

 later and attain therefore only an embryonic condition if they 

 continue development at all. (For facts see Pol, 1921 ; Mohr and 

 Wriedt, 1918.) These cases will be cited in a later chapter on 

 rate mutations. 



A complete survey of mutant types of animals and plants 

 might furnish innumerable such examples, which have been 

 described as abnormalities by arrest of development. One such 

 instance is to be found in the anomalies of the human eye as 

 analyzed by Waardenburg (1930). He analyzed thoroughly a 

 case of hereditary ptosis combined with different abnormalities 

 of the eyelids and lachrymal apparatus. By careful comparison 

 with the embryological facts, he came to the conclusion that in 

 this as well as in other hereditary abnormalities of the eye an 

 embryonic condition has been preserved as the result of a gene- 

 controlled disturbance in the interplay of developmental reac- 

 tions, of course followed by such adjustments as are forced upon 

 the organ by the further development of neighboring parts. (We 

 might point out here also the phylogenetic significance of such 

 facts. Waardenburg mentions the theory of Boek that human 

 morphology is a "fetalization" of the morphology of apes.) I 

 have quoted in this connection in a former book the fact that the 

 rudimentary wings of carabids represent the stage of pupal wings. 

 Such examples could be multiplied indefinitely. 



There can then be no doubt that the action of mutant genes is 

 very frequently of this type. In dynamic terms, it might be 

 described as an insufficient production of substances needed for 

 growth and differentiation, an insufficiency that reaches at a 

 definite point of development a subliminal condition instead of 

 coming up to the necessary threshold value. The basis for such 

 a description of the underlying process is derived from the exist- 

 ence of series of such effects with different times of onset of the 



