Primary Genetic Possibilities 431 



they would have the weak F(Y) from Hokkaido. But actually they 

 behave like strong females. The only explanation is that a strong F(Y) 

 transmitted occasionally to a Tokyo male, owing to non-disjunction in 

 his mother, enters a sperm which, upon union with an X-bearing egg 

 from the Hokkaido female, gives rise to a strong female, that is, Fst 

 (Y)Mw(X). It was this analysis which first suggested that F is located 

 in tlie Y-chromosome (1920c). (Later I thought for some time that F 

 was a cytoplasmic property, which left the present case unexplained. 

 I finally returned to the old interpretation; see 1942Z?. ) Here again we 

 face the same situation for our present problem. Only the F/M 

 balance agrees with the facts, and the sex-promoter genes-trigger 

 mechanism is ruled out. 



The same conclusion can be derived also from the facts of trip- 

 loid intersexuality in moths and especially Drosophila (Bridges, 1922). 

 We have already mentioned the loose way of describing the facts by 

 saying that sex in these triploids is determined by the relative number 

 of autosomes and X-chromosomes. This is a confusing way of saying 

 that in Drosophila the X-chromosomes carry the female determiners, 

 and one or more autosomes (see I 2 C d ee) the male determiners, 

 and that the normal balance mechanism M(autosomal)/F(X) or 

 M/F(X)F(X) can be changed, for example, by multiplying the auto- 

 some sets and (or) X-chromosomes, with the balance undisturbed or 

 disturbed, as the case may be. The result, normal sexes or intersexual- 

 ity, does not follow the multiplication of autosomes, as the trigger 

 theory requires, but exclusively the balance or imbalance between 

 autosomal and X-determiners. It follows that only our F/M balance 

 theory can explain the result, as both Standfuss (1914) and Bridges 

 (1922) concluded correctly. Thus we may regard the idea of sex 

 determination without F/M balance, according to what I called the 

 naive theory, as disproved. This also entails the idea, expressed by 

 Westergaard (1948), that the balance is between sex-chromosomal 

 trigger genes and autosomal sex-promoting genes. All the facts are 

 opposed to this, including those which Westergaard himself estab- 

 lished. To these we shall return later. 



