GENETIC EFFECTS IN MAMMALS 839 



with greater frequency in spermatogonia than in sperm, for the loss of 

 spermatogonia for given doses (Table 12-3) is much greater than would 

 be expected from the reduction in litter size produced by the same doses 

 given to sperm. Several factors could be involved. In the first place, 

 the spermatogonia are diploid and the sperm haploid. Furthermore, the 

 frequency of chromosome breakage, and the proportion of breaks that 

 result in lethal aberrations may be influenced by the state of the chromo- 

 somes, the phases of the mitotic cycle in the spermatogonia, and the 

 oxygen tension or other metabolic characteristics. The total effect of 

 these possible factors cannot be accurately estimated. All that can be 

 said is that there is still plenty of latitude for the assumption that more 

 dominant lethals are induced in spermatogonia than in sperm. 



If the reduction in litter size shown in Table 12-7 is real, and certainly 

 some effect of mutation would be expected, it could be attributed to 

 dominant lethal chromosomal or point mutations that are not eliminated 

 by germinal selection, to dominant subvital mutations, or, perhaps, to a 

 combination of these. The effect is apparently too slight, however, for 

 easy analysis of the time and nature of death of the missing individuals. 



The percentages of stillbirths and of postnatal deaths before 75 days of 

 age in progeny of poststerile-period matings are slightly, but not sig- 

 nificantly, higher than in the controls in Hertwig's (1938a) data on mice. 

 Strandskov's (1932) data on the guinea pig show no difference between 

 experimentals and controls in postnatal death before 30 days of age, but 

 the experimentals had a higher percentage of stillbirths and lower 0-day 

 and 30-day corrected weights. The differences are on the borderline of 

 significance and conditions that could have affected the 30-day weights 

 were not exactly matched in experimentals and controls. Some effect, 

 through the induction of dominant mutations, would be expected, but, as 

 with litter size, it is apparently too small for easy detection. 



Sex Ratio. Death of .embryos from dominant lethals could, through 

 differential mortality of males and females, result in a disturbed sex 

 ratio at birth. Certain types of chromosomal aberration, such as loss of 

 part or perhaps all of the X chromosome, could conceivably upset the 

 sex ratio without affecting survival. The available data do not present a 

 consistent picture. Parkes (1925), who exposed male mice to an X-ray 

 dose below that which produces temporary sterility, reported a barely 

 significant increase in proportion of males born from matings made from 

 to 4 days after irradiation (59.4 per cent of 133 animals as against 51.6 

 per cent of 735 controls) and a significant drop in proportion of males 

 born from 5- to 18-day matings (33.6 per cent of 143 animals). In the 

 offspring of still later matings (19 57 days), the sex ratio was normal 

 (54.4 per cent of 217 animals). Hertwig (1938a), however, found, for 

 male mice exposed to 400-1400 r, no effect on sex ratio at birth in the 

 progeny of presterile-period matings as a whole and no difference between 



