EVOLUTION 199 



and then only when the proper mating was made. Though 

 there is no direct support for this idea in the species where 

 the premises hold, there is some evidence that the reason- 

 ing is not wholly improhable. Bud- variations occur much 

 more frequently in heterozygotes than in homozygotes. 

 This simply means that bud-variations are brought to 

 light more frequently in heterozygotes than in homozy- 

 gotes : and a reason is not hard to find. Recessive varia- 

 tions are much more frequent than dominant variations, 

 and a recessive variation in a particular diaracter shows 

 only when the organism is heterozygous for that char- 

 acter. If a recessive bud- variation arises in a homozygote 

 and gametes are afterwards developed from the sporting 

 branch, it is not at all unlikely that the variation may 

 show in the next generation, but it wiU be attributed then 

 to gametic mutation. 



If, therefore, one is constrained to admit that the pre- 

 ponderance of the evidence points to practically the same 

 coefficient of heredity for both forms of reproduction, and 

 that variation in the sense of actual changes in germinal 

 constitution may occur with greater frequency in asexual 

 reproduction, if there be any difference at all between 

 the two forms, he is left with only one reasonable hypoth- 

 esis to account for everything, Mendelian segregation 

 and recombination. 



Mendelian heredity is a manifestation of sexusd re- 

 production. Wherever it occurs, there Mendelian heredity 

 will be found. Now if N variations occur in the germ- 

 plasm of an asexually reproducing organism, only N types 

 can be formed to offer raw material to selective agencies. 

 But if N variations occur in the germ plasm of a sexually 

 reproducing organism 2" types can be formed. The ad- 



