HEREDITY IN SOMATIC CELLS 



375 



I I I I i 1 I I I I i 



2 4 

 Stage 



8 10 12 



FIGURE 12.10. Isotope dilution curves on cells from an A^ donor. In (1), the 

 closed circles represent the results of subtracting from the experimental values that 

 value obtoined at stage 6. it shows that the agglutinable cells were lost at a 

 constant rate. In (2), the use of two specific agglutinins shows that the A j blood 

 had both A2 and O cells (from Atwood and Scheinberg, 1958, J. Cell. & Comp. 

 Physiol., 52, Suppl. 97; and Atwood, 1958, Proc. Natl. Acad. Sci. Wash., 44:1054). 



formation of homozygotes. It may be explained as a phenocopy and 

 have no real genetic basis, or it may be a true case of somatic mutation. 

 The bone marrow should behave formally like a chemostat overflowing 

 into the blood stream; with a constant mutation rate and no selection, 

 the number of mutant blood-forming cells would increase with age, per- 

 haps in a linear fashion. It can be calculated that a mutation rate of 

 ab(Hit 10~'^ per cell per division would be required to account for a 

 frequencv of 10~^ mutant cells at age 35. This rate is within the range 

 found in cultured bone marrow cells mutating to drug resistance 

 (Table 2.3). If the rate is calculated per hour, it becomes about 10 , 

 similar to the rates of mutation of bacteria and viruses. This raises the 

 question of whether the stability of genes in all organisms is about the 

 same, the calculated differences residing in the length of time required to 

 duplicate genes in different organisms. 



The process of somatic mutation mav be more readily studied in tissue 

 cultures where cells can be grown separately in suspension, plated out 

 to form colonies, and, in general, treated as bacteria. Puck has devel- 

 oped techniques for this purpose which originallv involved plating on an 

 irradiated feeder layer of other cells which could not grow but, nonethe- 



