104 



GERT BONNIER 



a relation of the type y = 4,3 + 0,2 z but that there is some relation 

 between y and z such as to make them increase at the same time. 



Taking it thus as granted that the above explanation of the diffe- 

 rent percentages of exceptions is the correct one there |s an inference 

 which is absolutely necessary to make. In the original Ä'-chromosomes 

 lie the already known factors for eosin and forked and there have 

 afterwards occurred new mutations (of lethal nature). The .Y-chromo- 

 some beha\ es with respect to crossingover as do other Ä':s since it crosses 

 over to the same extent as do ordinary Z:s, (see Bonnier 1922, where fi- 

 gures are given for different percentages of crossing over in .X). We have 

 therefore no right to believe that the genes in the X are of another kind 



II than in the ordinary A", but that in addition to the genes 

 I eosin forked and some lethals the A':s are loaded with the 

 I ordinary normal allelomorphs. As, however, the A- 

 I chromosome in the respect of producing exceptions be- 

 haves differently than do other A-chromosomes it must 

 necessarily be concluded that the difference between the 

 A:s and other A:s is a difference with regard to something 

 other than the genes. And since the different parts of 

 the A when of equal length seem to have the same in- 

 fluence upon the percentage of exceptions it follows that 



□ this »something» must be distributed all over the whole 

 A. b. " 



Fig. 1. Scheme chromosome. Then the necessary inference is: ihe 



of chromosomes chromosomes consist not only of the genes but of so- 



from the stand- „,p//„7,g (^/^^ which extends from end to end of the chro- 

 pomt of a gene- 

 basis. A Normal mosomes and in which the genes are so to sag embedded. 



chromosome, B I think that the word genebasis may be a suitable name 



for this new' component of the chromosomes. 



If we want to have a diagram of the chromosomes 



we have not to draw this diagram in the ordinary way as a chain of 



beads, but as a rod in which beads are embedded (fig. 1 A). The rod 



itself is then the genebasis and the beads are the genes. 



There are of course a number of consequences following from this 



supposition of a genebasis but I confine myself to pointing out only one 



of them. This concerns the problem of deficiency as studied by 



Bridges (1917) and Mohu (1919). The deficiency consists in that the 



consecutive genes of a part of the chromosome are »inactivated» or 



»lost». I think that the workers on deficiency agree in the assumption 



that there is a real physical loss. But if there is a loss this loss may 



as well be a loss of the genes only but not a loss of the genebasis. Then 



Deficient chro 

 mosome. 



