298 PHYSIOLOGICAL GENETICS 



regarding the number of episomes will therefore lead to results 

 exactly consistent wit h ( roldschmidt's calculations on the basis of 

 quantities. For eventual difficulties, the different episomes are 

 .it hand to be called in when a purely quantitative point of view 

 is difficult (Infrabar). This theory, which does not seem to have 

 more heuristic value than the others, has now lost its original 

 foundatioD since Bar has been proved to be a duplication of a 

 chromosome segment. To retain the terminology, one would 

 have to call the whole of the chromosome the protosome. 



4. THE GENE AS LOSS OF CHROMOSOME MATERIAL 



Serebrowsky (1929) pointed out that gene mutations may not 

 be changes within a so-called gene but actual losses of chromosome 

 material. He assumed that chromosomes tend to stick together 

 and later to break apart again, whereupon small segments are 

 lost. What appears as gene mutation would actually be a defi- 

 ciency. In fact, actual deficiencies, lethals, semilethals, and 

 visible mutations look like a series of different grades of the same 

 phenomenon, so that with large visible deficiencies at one end, 

 small deficiencies may be the other end of the series, i.e., recessive 

 mutations. Thus, assumptions regarding attachment and break- 

 age, inversions, translocations, and deficiencies are made different 

 aspects of the same phenomenon, and their phenotypic effects in 

 all cases are reduced to the action of a deficiency. In this group 

 would also be included the so-called gene mutations. Serebrowsky 

 does not commit himself as to how such a small deficiency 

 ( = recessive mutation) is to be understood in terms of genes. A 

 recent theoretical discussion by Hagedoorn (1934) may also be 

 interpreted as of a similar type. Stadler (1932) elaborated a 

 similar idea. He starts from the difficulties in proving that a 

 mutation is actually a chemical change within a gene. In fact, 

 many perfectly good mutations have later turned out to be 

 actual deficiencies. In experiments with X-ray induced muta- 

 tions, not only the rate of mutation is proportional to X-ray 

 dosage but also the rate of production of deficiencies. A similar 

 parallel exists between the reducing influence of dormancy of the 

 treated cells upon mutation rate and upon rate of chromosome 

 derangements. A discussion of many facts concerning mutation 

 in plants shows that all the results may be interpreted in terms of 

 deficiencies. The obvious difficulties to such a view derived 



