854 RADIATION BIOLOGY 



Table 12-11. The results already indicate that the relative frequencies 

 of viable, semilethal, and lethal types differ according to the locus. Most 

 striking is the uniformity of D-locus mutations. Not only are all of the 

 five tested mutations at this locus semilethal; they also exhibit the same 

 phenotypic effect: a coat color which is like that produced by the d 

 allele, but, combined with this, a curious behavior defect characterized by 

 convulsive fits exhibiting clonus of the limbs and opisthotonos of the body. 

 Furthermore, this phenotype is indistinguishable from that of the spon- 

 taneous Z)-locus mutation obtained in this investigation and of the spon- 

 taneous mutation found by Searle (1951). 



The question arises as to how many of the induced mutations scored by 

 the specific loci test are deficiencies. The following evidence bears on 

 this question, although it does not provide a definite answer. The fre- 

 quency of the homozygous lethal effect suggests that at least some of the 

 mutations may be deficiencies. The occurrence of three mutations that 

 appear to be intermediate alleles is presumptive, though not conclusive, 

 evidence of gene mutation in these cases. The most favorable loci for the 

 detection of deficiencies by phenotypic effect are the D and Se loci which 

 are closely linked (average crossover percentage 0.16). Of the total of 

 eight mutations obtained at these loci in the experimental group, none 

 shows the phenotypic effect that would be expected from a deficiency 

 involving the linked locus. 



HUMAN HAZARDS 



The genetic hazards of radiation in man have been discussed by 

 Haldane (1947), Muller (1950a, b, c; also see Chap. 7, this volume), 

 Wright (1950), and others. No attempt will be made here to review the 

 concepts of population genetics used or the resulting estimates of the 

 hazard, which have been calculated mainly on the basis of mutation 

 rates in Drosophila. The present section is limited to a brief discussion of 

 the application of the experimental results that have been presented in 

 this chapter. 



Considering, first, the dominant defects, such as lethality, sterility, and 

 partial sterility, that appear in the offspring following irradiation of the 

 later stages in spermatogenesis, it is well established that the rate of 

 induction of these is much higher in mice than in Drosophila. This would 

 be expected if most of them are due to major chromosomal aberrations, 

 for the haploid number of chromosomes in the mouse is twenty, while in 

 Drosophila melanogaster it is four. It is reasonable to suppose that, with 

 twenty-four chromosomes in man, the rate in man might be somewhat 

 higher than that in the mouse. Some of the effects, for example, death of 

 early embryos caused by dominant lethals or by aneuploid gametes from 

 translocation heterozygotes, might bring little or no distress, and might 

 pass unnoticed as individual occurrences, but the rate of induction of those 



