HEREDITY IN SOMATIC CELLS 



373 



methylcholaiithrciu' do not grow when transplanted haek into the 

 parental lines but do so onlv when transplanted into the hybrid line. 

 This is beeaiise eaeh parent was homozygous for either the H-2 or the 

 H-2' allele, while the hvbrid was a heterozygote, H-2" /H-2'. Therefore, 

 the tumor elieited antibodies in the parental hosts which lacked one or 

 the other gene and the corresponding antigen. But sometimes variant 

 cells arise in the tumors, allowing sur\i\al in one of the parental hosts; 

 their frequency is increased by X-rays. Serological tests indicated that 

 some of these variant tumors had lost the H-2" antigen, allowing them 

 to grow in the H-2'' /H-2'' parent (Figure 12.9). In model experiments 

 in\'ol\ing the artificial mi.xture of compatible and incompatible tumor 

 cells, it was shown that the compatible cells had an absolute selective 

 advantage and grew even when present in proportions as small as 4 X 

 10"', despite the destruction of their incompatible neighbors. As a con- 

 sequence, variation and selection seem the explanation. 



Variation in the constitution of tumors is of common occurrence; 

 usuallv their antigens are only a sample of those in the cells that 

 produced them. It is not at all sure that point mutations are the basis; 

 chromosomal changes seem usually involved, especially when there is a 

 great increase in the range of transplantabilitv. But e\en when specific 

 variants arise from controlled heterozygotes, deletions, somatic crossing 

 over, and other mechanisms are a priori as probable as point mutation. 



Parent a 

 H-2°/H-2° 



Transplant 

 takes 



_ Parent s 

 H-2' /H-2' 



/I 



/ I 



Transplant 

 fails 



FIGURE 12.9. Diagram of the consequence of somatic variation in a heterozygous 

 tumor. 



