306 GENE MUTATIONS CAUSED BY RADIATION 



manner (see below), tends gradually to level off and then even to sink 

 at very high dosage levels, levels resulting in a great mortality of the 

 germ cells or offspring. It seems reasonable to infer, as Hollaender has 

 done, that this flagging of the curve is caused, in part at least, by the 

 mortality being selective, for the distribution of ultraviolet can seldom 

 be made very even, and cell susceptibility also may vary. It is to be ex- 

 pected that the deleterious action of the radiation on viability would in 

 general be exerted more heavily against the same cells as have more 

 mutations induced in them, sometimes because these cells have received 

 more radiation and sometimes because they are in a more susceptible 

 condition. Moreover, in some material (that in which the effect of the 

 mutations can show relatively early, before the physiological effect of 

 the ultraviolet on viability has faded away) the mutations themselves 

 would give the cells, in their further development, a greater mortality 

 as compared with non-mutated specimens when they had at the same 

 time received a physiologically more effective dose of ultraviolet; this 

 too would tend to lower the apparent mutation rate more at higher 

 doses. There may in addition have been appreciably more "light re- 

 activation" at the higher doses in some of the experiments, and this 

 would have weakened the effective doses more just when they were in- 

 tended to be stronger. 



It is also conceivable, as an explanation of why the curve becomes 

 convex at higher doses, that ultraviolet of mutagenic wave length exerts 

 a second effect on the mutation process, similar perhaps to that of very 

 long ultraviolet and short visible light, so as to interfere with the pro- 

 duction (or to cause the reversal before their completion) of the very 

 mutations which this same mutagenic ultraviolet, presumably through 

 separate quanta, induces. In that case we should have to assume further 

 that this counteracting effect rises more steeply with the dose than the 

 mutagenic primary effect does. This would, for instance, be true if the 

 frequency of mutations primarily induced varied as (P, that is, as the 

 nth power of the dose, because of n hits being required for a mutation, 

 whereas the final or net frequency of mutations, that remaining after 

 the counteracting quanta had taken effect, varied as the product of (P 

 times e''^ (where A; is a constant) . This formula would follow the principle 

 which appears to operate in "reactivation" by visible and long ultra- 

 violet light, as judged, for instance, by Novick and Szilard's results 

 (see below), although of course in the case of visible and long ultra- 

 violet light reactivation it would be necessary in this formula to sub- 

 stitute a different letter for the second d, representing the amount of 

 that radiation, since the first d would represent only the amount of 

 mutagenic radiation. It is true that this interpretation has the objec- 



