CHROMOSOME ABERRATIONS IN ANIMALS 657 



and Robson, 1946; Auerbach, 1949, 1950; Kaufmann, Gay, and Roth- 

 berg, 1949), and in chick fibroblasts by urethane (Paterson and Thomp- 

 son, 1949). 



Such results have raised the question whether breaks in chromosomes 

 are ordinarily produced by a series of reactions originating in remote 

 parts of the cell. A. R. Whiting (1949, 1950) examined this question in 

 considerable detail. Her experiments on Habrobracon confirm and extend 

 the earlier findings on various species, including D. melanogaster (reviewed 

 in Schultz, 1936). Cytoplasmic injury produced in eggs by very intense 

 doses of radiation inhibits the development of all embryos. After lower 

 doses, however, which still may be twenty times greater than that 

 required to induce dominant lethals in all the egg chromosomes, andro- 

 genetic males may develop (from nonirradiated chromosomes in X-rayed 

 cytoplasm). No mutations are induced in these males, which are 

 normal in morphology and fertility and produce fully viable progeny. 

 If irradiated cytoplasm exerts any mutagenic action, it must be effected 

 within a shorter period than that tested in these experiments. Auerbach 

 and Robson (1947) also concluded that there was no delayed effect on 

 untreated chromosomes of cytoplasm treated with mustard gas. Other 

 studies indicate that the lethal effects of radiation, such as killing of 

 Drosophila eggs, depend primarily on nuclear damage (e.g., Langendorff 

 and Sommermeyer, 1940). 



It appears improbable, therefore, that ionizing radiations or chemical 

 mutagens effect genetically significant types of chromosome breaks 

 through the accumulation of toxic substances in the cytoplasm. The 

 fact that chemicals can induce rearrangements similar to those induced 

 by radiations may merely indicate that breaks are produced with com- 

 parable potentialities regardless of the agent used in their production; it 

 does not, as some authors have assumed, dispose of the possibility that 

 the sequence of events leading to breakage can originate within the 

 chromosome. Similar end results, as represented by a series of breaks or 

 rearrangements, may conceivably be mediated through a variety of 

 channels. A more specific definition of the radiation-induced reaction 

 system therefore depends on more precise information concerning the 

 effects of ionizations on the genetically active materials of the chromo- 

 some and on other cellular materials. This being the case, the question 

 whether an effect is localized or remote is reduced to a choice of prob- 

 abilities between the effectiveness of a sequence of events originating in 

 the chromosome and that of one initiated elsewhere in the cell (Kauf- 

 mann, 1948a). 



The target theory, in its more general terms, is formulated in accord- 

 ance with the first of these alternatives. Primary production of breaks 

 occurs with a frequency that is proportional to dose over a wide range of 

 wave lengths, including X rays and y rays. The effect is independent of 



