BIOCHEMICAL MODELS OF HETEROSIS IN NEUROSPORA 



205 



modified), and in addition a second mutant gene, S, which was presumably 

 responsible for the change in growth (Table 12.1). 



The new mutants appearing in the heterocaryons have been called sup- 

 pressors because they overcome the deleterious effect of the sulfonamide- 

 requiring gene in heterocaryons. Actually they are not like the usual suj)- 

 pressors, because in homocaryotic strains which also carry the sulfonamide- 

 requiring gene they do not result in wild type growth. 



Growth characteristics of strains homocaryotic for four of these suppres- 

 sors, with and without the sulfonamide-requiring gene, are represented in 



TABLE 12.1 



DISTRIBUTION OF NUCLEI IN 

 THE HETEROCARYONS REPRE- 

 SENTED IN FIGURE 12.3 



Figure 12.4. From these growth curves it can be seen that wild type (+, +) 

 is neither inhibited by sulfanilamide in a concentration of 2 X 10~^ M, nor 

 stimulated by />-aminobenzoic acid in a concentration of 10"'* M when grown 

 at 35°, and is only slightly inhibited by sulfanilamide at 25°. At 35° growth of 

 the sulfonamide-requiring strain (sfo, -\-) is stimulated by sulfanilamide and 

 inhibited by ^-aminobenzoic acid, though neither substance has an appre- 

 ciable effect at 25° in the concentrations used. 



The suppressor from tube 1 (+, ^-1) does not grow at 35°, and grows slow- 

 ly on all media at 25°. The suppressor from tube 2 (+, 5-2) differs from wild 

 type principally in taking longer to attain its maximum growth rate, though 

 there is also some stimulation by sulfanilamide at 35°. When combined as a 

 double mutant with the sulfonamide-requiring gene (sfo, 5-2), it almost ap- 

 proximates the growth of wild type. The suppressor from tube 4 (+, 5-4) 

 differs from wild type in being stimulated by />-aminobenzoic acid and in- 

 hibited by sulfanilamide, the inhibition being stronger at 25°. In combination 

 with the sulfonamide-requiring gene (sfojSA) it resembles the sulfonamide- 

 requiring strain itself except that there is a long lag phase on sulfanilamide 

 at 35°, and inhibition at 25°. The suppressor from tube 6, either alone 



