CHROMOSOMES AND GENES 



61 



normal pairing. (These are thus far the 

 only objects in which such a study can be 

 made.) But there have come to light some 

 new facts regarding mutation which are 

 bidding fair to throw light upon the nature 

 of those mutations which are called point 

 mutations because no chromosome break has 

 been discovered, as yet, at their locus. Mu- 

 tation was always assumed to be a rare hap- 

 hazard process, occurring at random in one 

 or another chromosome at different times of 

 the developmental cycle. During the past 

 ten years, however, a series of cases of mass 

 mutation, closely paralleling each other in 

 their details, have been found. The first 

 case found by myself was unfortunately not 

 recognized as such, as it happened in a tem- 

 perature-experiment and was attributed to 

 the action of heat, but wrongly so, as can be 

 shown from the pedigrees. But two more 

 parallel cases have since been found in the 

 same Drosophila line (Plough and Holt- 

 hausen, Demerec), two more by the present 

 author in different lines and one by Vala- 

 dares, again in a different line. In addi- 

 tion, a statistical study of mutation in Dro- 

 sophila on a large scale (Spencer) has 

 revealed that mutation occurs not at ran- 

 dom but in clusters. Looking for some 

 feature in common to all these cases we 

 realize that in three of the cases the line 

 which produced mass mutation contained 

 major chromatin rearrangements, translo- 

 cations, and inversions. The three other 

 cases are derived from Florida stock which 

 since was found to contain a large inversion. 

 In one of my cases the complete history is 

 known and the analysis (not yet finished) 

 shows that with the process of mass-muta- 

 tion the previously present chromatin rear- 

 rangements (very small ones, but detectable 

 in the salivary glands) had changed. 

 Though the analysis is not yet completed, 

 everything points to very small transloca- 

 tions, inversions, duplications as the actual 

 nature of some recessive mutants. As 

 translocations are generally considered to 

 arise through illegitimate crossing-over, one 

 might assume that the rearrangements 

 which prevent legitimate crossing-over (in- 

 versions, translocations) tend to increase 



the tendency for illegitimate ones. I am 

 fully aware that this statement is not as 

 concrete as it ought to be, but I hope that 

 the time is not too distant when it will be 

 specified in detail. (Since this was written 

 another case of high mutability accom- 

 panied by the presence of rearrangements 

 in the mutable stock has been described by 

 Tiniakov.) 



There is an additional very interesting 

 fact which strongly suggests the correctness 

 of this interpretation. Beadle described in 

 maize a mutant locus, sticky, which causes 

 some physical condition in the cell which re- 

 sults in a tendency of the chromosomes to 

 stick together and to break irregularly. 

 Therefore in the presence of this mutant 

 locus, also, the number of translocations 

 increases immensely and simultaneously the 

 number of regular mutants. Interpreting 

 this fact from the standpoint of the classic 

 theory of the gene, one has to assume that 

 one of the functions of the mutant locus, 

 sticky, is to make other genes mutate. Ac- 

 tually this (to my mind erroneous) conclu- 

 sion was drawn and the same was also done 

 for some of the other cases of mass-mutation 

 (Demerec), though without any proof. (I 

 wonder what the function of the normal 

 allele of the mutant gene for mutation 

 would be. The normal allele of white eyes 

 is supposed to control normal eye color or 

 take part in its control, as evidenced by 

 deficiencies at all so-called hypomorphic 

 loci, if I accept the explanation in terms of 

 the classic theory for argument's sake. 

 Logically, then, the allele of the gene for 

 mutation would prevent mutation.) But it 

 seems rather obvious in the ** sticky" case, 

 that the same stickiness which produced the 

 translocations also produced the mutations. 

 In other words, the mutations were not 

 chemical events within genes but mechan- 

 ical changes in the chromosomes, i.e., 

 changes of pattern alone. Facts are indeed 

 beginning to accumulate which strongly 

 support such an interpretation. I mention 

 the claim that induced chromosome breaks 

 are most frequently located in sections of 

 the chromosomes, which are also known for 

 a high frequency of point mutations (Timo- 



