48 



Mr. H. Onslow. 



instability of the inhibitor, which spontaneously decomposes in 48 hours at 

 room temperature. 



2. Distribution of the Inhibitor in the Skins of Agouti and Yellow Babbits. 



An attempt was made to extract a ferment fluid from agouti rabbits. On 

 two occasions a large number of tubes were prepared from these rabbits, but 

 in no single case was there any sign of oxidation. The most probable 

 explanation of this seemed to be that the white belly of the wild rabbit 

 which is well known to be dominant over self-colour, contained sufficient 

 inhibitor to prevent oxidation. The skin of the bellies of some more agouti 

 rabbits was therefore separated from the skin of the backs, and an extract 

 prepared from each portion. It was now found that the skin of the backs 

 contained an active tyrosinase apparently similar in all respects to that of 

 black rabbits, whereas the skin from the bellies contained so much inhibitor 

 that 20 per cent, of the extract was sufficient to prevent oxidation taking 

 place in the ferment fluid extracted from the backs. The white bellies of 

 yellow rabbits were found to contain a similar inhibitor. 



It seems indubitable, therefore, that whenever rabbits, and probably also 

 other animals, have dominant white coats, or coats which have a white 

 pattern that behaves as a dominant to self-colour, the dominance is produced 

 by the presence of an inhibitor or an ti- tyrosinase in the skin of the animals 

 in question which can prevent any colour being produced by the existing 

 chroniogenic system. 



V. The Cause of Recessive Whiteness. 

 1. The Distribution of Enzyme and Chromogcn. 



Having shown that dominant whiteness is caused by the presence of a 

 chemical inhibitor or an ti- tyrosinase, it remained to indicate the cause of 

 recessive whiteness. It is clear that recessive whiteness cannot be due to 

 the same factor as dominant whiteness, for it is logically impossible that a 

 form of whiteness caused by an inhibitor can be recessive to colour, since 

 it is not conceivable that the union of two germ-cells, one carrying 

 potentially a chemical inhibitor and the other the full mechanism of 

 pigment-production, could result in a pigmented animal ; unless, indeed, 

 the potentially pigmented germ-cell also contained a factor which neutralised 

 the effect of the inhibitor. Such a supposition is hardly an economy of 

 hypotheses. 



If, then, recessive whiteness is not caused by an inhibitor, it must be due 

 to the lack of one or both of the factors necessary for pigment-production, 



