GENETICS OF INFECTIOUS DISEASES 387 



The L mice on the other hand were less resistant, 7.6 per cent. This difference is 

 seemingly important, although numbers of mice are not large and other factors 

 besides binomial variations contribute to the real variance of data dealing with problems 

 of disease. 



The differences between the resistant and susceptible strains for either period were 

 pronounced. Confining attention to the first three hybrids, S x RI, RI x S and 

 BR x S, the results showed the hybrid resistances to be closely similar to those of their 

 inbred parents, although they were, in each case, a little less resistant, 9 per cent. This 

 was convincing evidence for the similarity of the genes making up the relatively resistant 

 strains. The results did not indicate heterosis. Rather they suggested partial domi- 

 nance for some of the genes controlling resistance. 



The hybrids SxL, LxS, SxBa, and Ba x S represent extreme crosses of 

 resistant x susceptible. They were only 6 per cent less resistant than the resistant 

 parental strain. Dominance of most genes for resistance was indicated. There was 

 no significant evidence for the reciprocal crosses being different from each other. In 

 mice the chromosomal arrangement is XY for the male and XX for the female. The 

 male progeny received all AMinked genes from the mother, whereas the females had an 

 X chromosome from each parent. Any major factors for resistance on the X chromo- 

 somes should make corresponding changes in the survival ratios of the sexes in the 

 reciprocal crosses. As Hetzer showed this was not the case. However, there was a ten- 

 dency for the females to have a higher survival than the males^ but the sex differences in 

 survival extended to all matings and not just those which were diagnostic of sex linkage. 

 The equality of the resistances of the hybrids further emphasized that resistance or 

 susceptibility to this disease was not due to a maternal effect but to inheritance being 

 transmitted by both sexes. Passive immunity carried through the egg cytoplasm, the 

 fetal circulation, the colostrum, or other maternal environmental effects was ruled out 

 as a factor materially influencing resistance. 



The crosses of mice of the L strain mated with those of the Ba strain represented 

 the crosses of two highly susceptible strains. The resulting hybrids' resistances were 

 greater than either parent's and by a noticeable amount. This result indicated that in- 

 bred strains L and Ba possessed genes for resistance even though they themselves were 

 quite susceptible. These genes complement each other to give increased resistance 

 to the F 1 progeny. This is in contrast to the results for the crosses of the resistant strains. 

 These crosses dropped slightly in resistance. The comparison between the two 

 classes of hybrids could be used against the argument that the results of the L x Ba 

 crosses were due to heterosis. However, that reasoning may not hold, for data have 

 been collected which indicated that heterosis may be genotype specific. 



The backcross data gathered by Hetzer 573 while in this laboratory further sup- 

 ported these views. The main feature of these tested backcross animals was the further 

 regression of their S. typhimurium resistances toward those of the susceptible strains. 

 This places their sensitivity to typhoid as intermediate between those of their resistant 

 and susceptible grandparents. Segregation of factors for resistance and susceptibility 



