THE GENERAL ASPECTS OF HEREDITY 17 



worked out quite independently of genetic experi- 

 ments, but they furnish precisely the mechanism 

 required to explain Mendelian behaviour, although 

 the main facts of their history were known before the 

 rediscovery of Mendel's laws in 1900. The number of 

 freely assorting groups of Mendelian characters in a 

 species should therefore be the same as the number 

 of pairs of chromosomes, and the experimental work, 

 particularly with the fruit fly Drosophila, clearly 

 indicates that this is the case. 



Differences in the chromosomes in crossed races 

 appear to determine the different types and combina- 

 tions of characters which arise in the offspring. It 

 thus appears that Mendelian differences in general 

 have originated as mutations, probably through an 

 alteration in a portion or locus of a chromosome. That 

 the differences which arise in this way are inherited 

 as Mendelian factors results, then, from the manner 

 of distribution of the chromosomes in the reduction 

 divisions, when the nuclei of the germ cells are formed. 

 Mutations seem to arise in the germ plasm at relatively 

 infrequent intervals. They may then be handed 

 down to later generations for an indefinite period. 

 In some cases the same mutation appears indepen- 

 dently more than once. 



Let us now consider the inheritance of a recessive 

 Mendelian character. Feeble-mindedness ma}'" be 

 taken as an example, for it appears to be generally 

 inherited as a simple Mendelian recessive. Con- 

 structing a diagram (Fig. 5), we see that all the 

 germ cells of a feeble-minded person will carry the 

 factor for feeble-mindedness, since the character 

 is recessive. 



If mated with normal, the children will all be normal 

 for the same reason, and the defect will seem to have 

 disappeared. But these normals will all be hetero- 

 zygous, carrying the defect for feeble-mindedness in 



