HYBRID VIGOR IN DROSOPHILA 



481 



There are three major hypotheses to account for the vigor of race crosses. 

 One hypothesis assumes an as yet unexplained physiological stimulation re- 

 sulting from the union of gametes of unlike origin. The second hypothesis at- 

 tributes hybrid vigor to the union of gametes carrying difTerent favorable 

 dominant genes for vigor, which cover up defects which may exist in each of 

 the original parent races. The third hypothesis also depends on genie action. 

 It assumes that the vigor of the hybrid comes from the association of unlike 

 alleles brought in from the two parental races, these unlike alleles are postu- 

 lated as contributing different, as well as like, chemical or physical stimula- 

 tions favorable to the vigor of the hybrid. The results of these experiments 

 presented in Table 29.2 are in favor of a genie basis rather than a physio- 

 logic stimulation as the cause of hybrid vigor, since throughout this work, 

 diverse cytoplasm has shown less yield than like cytoplasm when put on a 

 background of homozygous or inbred inheritance. 



INBREEDING EFFECTS ON HETEROSIS AS RELATED 

 TO DEFECTIVE GENES 



The creation of homozygous types tests the parent race for heterozygosity 

 of particularly undesirable genes, lethals, and semi-lethals. Table 29.3 shows 

 the results obtained in mating the homozygous races. 



TABLE 29.3 



GENOTYPES OF INBRED RACES FOR VIABLE, LETI|^, 

 AND RECESSIVE VISIBLE ALLELES 



Race 



Princeton 

 Inbred. . . 

 Florida. . . 

 Florida. . . 



Line 



1 



9 



5 

 2 



No. 

 Lethal 



9 







98 







Lethal 



7 



17 

 20 

 12 



Recessive 

 Visible 





 



2 

 2 



Total 

 Isolation 



16 



17 



118 



14 



The lethals observed were all in chromosomes 2 and 3. They range in fre- 

 quency from 17 per cent for one race to 100 per cent for another. The visible 

 recessives picked up were also semi-lethal. The mathematical model em- 

 ployed in inbreeding calculations postulates random recombination and fer- 

 tilization. Conclusions are misleading when these postulates are not met. The 

 above evidence for mechanisms to maintain heterozygosity in races even 

 though the matings are of relatives as close as continued full brother X sister 

 seems unmistakable. The defective genes are in the races. Residual defective 

 genes can contribute both toward and away from greater heterotic effects in 

 particular crosses. As these defective genes arise ultimately by mutation and 

 as the number of the genes is large, the ultimate possible genetic changes are 

 appreciable and may be an important force toward heterosis. 



