HEREDITABY TYPE OF CHARACTER STUDIED. 59 



human hand. When we further take into account the extreme varia- 

 bility in human hands, not only in general, but also within a strain 

 where a characteristic familiar type is inherited for generations, it seems 

 justifiable to suggest that the different individuals also carry numerous 

 modifying genes which may influence the appearance of other charac- 

 ters — ^for instance, the malformation we are here dealing with. 



Let us see if the occurrence of two types in our case may be explained 

 on the hypothesis that some of the normal individuals who married into 

 the family have been heterozygous for a specific modifier, enhancing 

 the effect of the principal gene. 



Suppose this modifying gene is dominant: The principal gene "B" 

 causes a shortening of the second phalanges of the indices (B-type 

 brachyphalangy). The specific modifier "Mb" enhances the effect of 

 B, altering the character into the very short type (B !-type), which is 

 thus a double dominant form. 



Applied to line 1 (text-figure 2) the B !-type brachyphalangous 11.5 c? 

 must have been of the constitution B Mb- Some of his children by 

 his second marriage with a normal wife will receive both B and Mb 

 and be of the B !-type (115.4 cT, 115.6 cf, 115.8c?'); some will receive 

 only B and be B-type brachyphalangous (115.5 cT); and some will 

 receive only Mb or neither B nor Mb and in both cases be normal 

 (115.3 cf and 115.7 9 ). The children of the first marriage of 11.5 cf with 

 his cousin 17.1 9 , who for reasons given above is supposed to have been 

 heterozygous for the principal gene B, may get this gene from one or 

 the other parent and be B-type brachyphalangous (115.1 9) or from 

 both (115.2 9 ; cf . pp. 28-29) . They, too, may or may not get the modi- 

 fier from their father, involving the eventualities just mentioned.^ 



In two cases within this Une (115.5 cT and 1151.2 9 ) B-type brachy- 

 phalangous individuals have a B !-type brachyphalangous child. Here 

 the other, the normal parent, must have been heterozygous for the 

 modifier Mb in order to establish the BMb combination causing the 

 B !-type brachyphalangy. 



The two genes B and Mb can not be supposed to be linked. Not 

 only is the chromosome number in man so high that such a linkage is 

 a 'priori extremely improbable according to chance, but the striking 

 contrast in the distribution of the two types within the two fines here 

 recorded is decidedly against a linkage hypothesis. 



With regard to line 9, where we have only one certain case of B '.-type 

 brachyphalangy against 10 cases of the B-t3rpe, we must assume that 

 the individual 19.4 9 has received only the principal gene B and not 

 the modifier Mb from her father. The only known case of B !-type 

 brachyphalangy within this line (1942.19) results from the first 

 marriage of the B-type individual 194.2 cT. It is interesting to notice 



1 The Bemi-lethal effect in one of these children (115.2 9 )■ interpreted as due to a homozygous 

 condition of the principal gene for brachyphalangy, might also be attributable to a homozygous 

 condition of the modifying factor combined with the heterozygous condition of the main gene. 



