auerbach: effects of chemicals 131 



consequence of their delayed action, if it is assumed that latent 

 breaks in the same chromosome have a sweater chance than latent 

 breaks in different chromosomes to open in the same cell cycle (81). 



Storing of mustard gas-treated spermatozoa in the seminal 

 receptacles of ? 9 did not affect the frequency of sex-linked lethals, 

 although calculations showed that the increase should have been 

 perceptible if delayed mutation had occurred at the same rate as 

 delayed breakage (10). Yet it is known that mutation is often delayed 

 after mustard gas treatment (4). It appears, therefore, that delayed 

 gene mutation requires replication of the chromosome, while 

 delayed breakage does not. If this can be firmly established, it will 

 form a distinguishing feature between chemically induced intergenic 

 and intragenic changes in Drosophila. 



Even if the mechanisms, by which mustard gas produces gene 

 mutations and chromosome breaks should differ in their final 

 stages, they must have a common initial step. This follows already 

 from the previously mentioned experiment in which it was shown 

 that the frequency of translocations increases as the square of the 

 frequency of lethals (68). It is further substantiated by the find- 

 ing that during the late spermatogonial stage, which is the most 

 highly sensitive one to the mutagenic effects of mustard gas, lethals 

 and breaks leading to translocations increase proportionally in 

 frequency (87). 



Minute deficiencies and other minute rearrangements occupy 

 a somewhat intermediate position between gene mutations and 

 large chromosome rearrangements. This is so in radiation muta- 

 genesis, where the frequency of minute rearrangements increases 

 linearly with dose, that of large rearrangements more nearly as 

 the square of dose. It is also so in chemical mutagenesis, where 

 compounds that are inferior to X-rays in the production of large 

 rearrangements may yet be superior in the production of minute 

 ones (36, 81). It is possible that a proportion of minute deficien- 

 cies is produced not by breakage and reunion but by some other 

 mechanism such as unequal crossing-over, or errors in chromosome 

 replication; but this is certainly not true for all of them, and probably 

 only for a small minority. Reverse repeats, e.g., cannot arise without 

 previous chromosome breakage, and they have been found repeatedly 

 after exposure of Drosophila to chemical mutagens (59, 67, 81). The 



