188 Nature of the Genetic Material 



sented as the classic and the modern views would, then, be that the 

 former deals only with the operational, the latter with the hypothetical, 

 gene and, in this sense, both can be right. In view of the facts 

 discussed, I have my doubts whether this philosophical solution of the 

 differences is possible. It seems to me that both views are of the 

 operational type, but the classic one is simply more primitive. This is 

 what I meant when I repeatedly emphasized that all of classic genetics 

 can be described in terms of the corpuscular gene; but, when it comes 

 to the question what this gene is materially, the facts force us to give 

 up this simple notion. Actually, Stadler's own important work is 

 witness to this. But, after all, the question of definitions may be left 

 aside and the problem treated pragmatically. 



I mentioned that there are still adherents of the idea that a 

 position effect break makes a nearby gene mutate. It has long since 

 been shown by Dobzhansky, Panshin, and Catcheside that a locus 

 showing position effect may be removed from the break and then 

 ceases to act like a mutant (using the old way of expressing the facts). 

 It might be answered that this involves a return mutation, but such an 

 answer could hardly be taken seriously. The whole idea explodes if 

 the position effect of a deficiency is contemplated, especially the 

 homozygous deficiencies with typical mutant action. The gene which is 

 supposed to mutate to and fro is not there at all. It is the same set of 

 facts, completely ruling out the interpretation of ordinary position 

 effect, which is most popular with authors who try to save the classic 

 concept of the corpuscular gene. They assume that the break, or the 

 new neighborhood in case of translocation or inversion breaks, 

 inhibits the action of the nearby gene so that it does not produce or 

 produces less of its typical reaction product. But if there is no "gene" 

 there? The only way out of this dilemma would be to declare that the 

 deficiency effects are something completely different. Taking the 

 yellow locus as an example, we might say that all residual heredity 

 makes for yellow color but that the gene +^ prevents this. If this 

 gene is taken away, yellow must appear. We must consider all the 

 mutant loci known to act like yellow in order to realize that such an 

 "explanation" amounts to no more than sophistry. 



An important role in the detailed discussions was played by the 

 series of more or less small chromosomal sections within which any 

 visible or invisible change of pattern produces a mutant effect. All 

 these effects behave like multiple alleles; but some pattern changes 

 (breaks) at a distance from the section in question (the overlap 

 effect) can still produce the allelic effect. We should have more in- 



