412 THE HEREDITARY FACTORS AND DIFFERENTIATION 



offspring 75 per cent, will produce dextral and 25 per cent, will 

 produce sinistral forms. It is clear that segregation has taken place 

 in the snail in question, but the dextral-determiner has acted upon 

 the cytoplasm of the oocyte before maturation in such a way that, 

 regardless of whether the dextral-determiner or its sinistral allelo- 

 morph has been extruded with the polar body, the embryos into 

 which those oocytes will develop when matured and fertilised 

 will be dextral. Owing to segregation, 25 per cent, of these embryos 

 will possess the sinistral-determiner only; their oocytes will be 

 subjected to the action of this sinistral-determiner, and all their 

 offspring will be sinistral. 



A similar case is found in silkworms. Here, the pigmentation of 

 the serosa membrane of the embryo is determined by the mother's 

 genetic constitution, and not by that of the embryo. MendeHan 

 segregation for this character occurs, but a generation later than for 

 ordinary characters.^ 



§7 

 In other cases, precursor substances may be formed in the cyto- 

 plasm of the egg under the influence of the maternal gene-complex. 

 An example of this is found in Gammariis. A mutant type known 

 as white body contains no carotinoid pigments, neither red in the 

 eyes nor green in the body : it is recessive to the pigmented type. 

 If a male of the white-body type is crossed with a red-eyed green- 

 bodied female, the offspring are red-eyed and green-bodied from 

 the start. But if the reciprocal cross is made, the young begin their 

 career without any carotinoid pigment, and the eyes and body 

 darken to the normal red and green shades only after some time. 

 In this case it would appear that a gene controls the production of 

 substances needed for the making of red and green pigment. When 

 these substances are absent from the egg, the dominant normal gene 

 introduced from the father takes time to produce these pigment- 

 precursors. But if the mutant white-body gene is introduced from the 

 father and the normal allelomorph from the mother, the precursors 

 have been already manufactured by the mother and a store of them 

 is present in the egg-cytoplasm." It is probable that the white-body 

 mutation renders the animal incapable of utilising carotinoids. 



1 Tanaka, 1924. ^ Sexton and Pantin, 1927. 



