224 Cytoplasm as Seat of Genetic Properties 



explained by gene mutations (some with similar eflFects had been 

 found ) of the type of the so-called unstable genes which we discussed 

 as position effects. These, as we have seen, can lead to variegations 

 on the basis of threshold conditions (see I 2 C d bb). But the results 

 of these special experiments agree best with Ephrussi's explanations 

 given above, and we do not need to present them in detail. 



In evaluating these important and beautifully analyzed facts for 

 the problem of plasmon action of the substrate or particulate type, I 

 should like to state that the description of the facts in terms of mu- 

 tation, mutagenic agents, and even loss mutations — though perfectly 

 justified in a purely descriptive sense, if we define mutation as any 

 hereditary change — is apt to prejudicate a definite type of interpre- 

 tation. In his last book (1953), Ephrussi himself mentions (fn., p. 34) 

 this objection, but prefers to hold to what I consider an objectionable 

 terminology, namely, in terms of plasmagenes. To make my point 

 clear, I mention a well-known cytological fact which closely parallels 

 the features of this case. It shows that a description of such processes 

 without using misguiding genetic terms may clarify the problem and 

 simultaneously prevent the suggestive implications based more on 

 terminology than on the naked facts. It is known that in the sperma- 

 togenesis of the aphids a maturation division occurs in which one 

 spermatocyte receives the X-chromosome, and is female-determining; 

 the other is without X and should be male-determining. But this divi- 

 sion is an unequal one for the cytoplasm so far as the major part of it 

 goes into the female-determining daughter cell together with all the 

 mitochondria. The small cell without mitochondria degenerates, ob- 

 viously because of the absence of the respiratory enzymes. Theoreti- 

 cally, it is possible that the small budlike spermatid could survive and 

 end its cycle as a somewhat pathological cell. If this were so we would 

 have a complete parallel to the behavior of the yeast. We might call 

 the unequal division a mutation, and even a loss mutation as far as 

 the mitochondria are concerned, though this would only obscure the 

 understanding. 



This example is much more than a chance similarity. It is a clear 

 hint that an unequal division involving the unequal distribution of a 

 cytoplasmic component, the mitochondria, is a cellular possibility 

 which may be caused by different external or internal agencies. The 

 work of Winge and Laustsen (see II 2 C a) clearly suggests the hypoth- 

 esis that in the present case the mitochondria, the carriers of respira- 

 tory enzymes, are the unequally distributed cytoplasmic particulates. 



However, I want to emphasize that, in continuing the use of the 



