GENETIC CHANGE AND EVOLUTIONARY CHANGE 423 



Thickened skin on the sole of the human foot, calluses on the "knees" of 

 the forelegs of the wart hog, calluses on the front and rear ends of the 

 body of an ostrich are examples. The skin on all these areas is found to be 

 thickened before birth. How can the origin of such hereditary thickenings 

 be explained? It is noteworthy that while these thickenings are hereditary 

 they are of such a nature that they would have been produced in direct 

 response to the environment if they had not been. Use of the human foot, 

 for example, causes the skin on the sole to thicken. 



How can we visualize the origin of an inherited thickening of the skin 

 at a point where friction will later be applied? In the first place we may 

 note that the ability of the skin to thicken in response to friction is un- 

 doubtedly determined by the genotype. If we knew more of the genetics 

 of the trait we should probably find that different genotypes vary in the 

 amount of friction needed to "trigger" the production of a certain amount 

 of thickening. Let us imagine an ancestral population in which the individ- 

 uals are born with thin skin on the soles of the feet. It would be of advan- 

 tage to develop thickening as rapidly as possible after birth, i.e., in re- 

 sponse to a very small amount of friction (or none at all! ). As a possible 

 intermediate step we may visualize a situation in which genotypes resulting 

 in production of maximum thickening in response to minimum friction 

 would be favored. The next step would be elimination of the need for any 

 stimulation whatever by friction, for as Medawar ( 1951 ) has stated, "if it 

 is advantageous to have thickened feet at all, it will be advantageous to 

 have them ready made when the foot is first put to the ground." How can 

 this last change be brought about? Formerly friction "pulled the trigger." 

 Now that it has become advantageous to have thickenino developed before 

 birth, natural selection will favor a genetic change which will result in the 

 taking over by some internal factor of this function of pulling the trigger. 

 This factor may be some inducing force operative upon the locahzed areas 

 of the skin as they develop in the embryo. Perhaps the original norm of re- 

 action included the possibility that thickening might arise as a result of 

 either external or internal stimuli; if so, development has now become 

 canalized so that the internal stimulus is the one regularly operative. Or 

 perhaps the internal factor which now acts as a trigger arose as the result 

 of one or more mutations. In any case, the adaptation which formerly had 

 to be acquired by each individual for itself (exogenous adaptation or ac- 

 commodation) has become hereditary in the sense that no external force is 

 any longer necessary to call it into existence. White and Smith (1956) have 

 called this phenomenon ontogenetic assimilation. 



Waddington (1953, 1956, 1960) has performed experiments affording 



