BIOCHEMICAL MODELS OF HETEROSIS IN NEUROSPORA 207 



(-|_^ 5.6) or in combination with the sulfonamide-requiring gene (sfo, 5-6), 

 grows very poorly at 35°. 



Of those illustrated, suppressors numbered 4 and 6 are perhaps the most 

 significant to the present discussion. When combined with the sulfonamide- 

 requiring gene (sfo, SA and sfo, S-6), neither grows well on minimal medium 

 at 35°. Yet heterocaryons between either of these double mutants and the 

 sulfonamide-requiring strain are enabled to grow quite well under those 

 conditions. In these heterocaryons the sulfonamide-requiring gene is present 

 in all nuclei, in some of which it is combined with a suppressor. The suppres- 

 sor is not capable of overcoming the ill effects of the sulfonamide-requiring 

 gene when present in all nuclei, but is effective when present in only some 



of them. 



Biochemical Basis for the Sulfonamide-requiring Character 



This seeming paradox becomes less important once the nature of the reac- 

 tion controlled by the sulfonamide-requiring gene is understood (Zalokar, 

 1948, 1950; Emerson, 1950). The diagrams in Figure 12.5 illustrate some of 

 the important reactions involved. There are a large number of amino acids, 

 vitamins, components of nucleic acid, and so on, that are essential to growth. 

 But we shall consider only two amino acids, methionine and threonine, and 

 the vitamin />-aminobenzoic acid. Para-aminobenzoic acid is involved in a 

 number of reactions essential to growth, one of which is the final step in the 

 synthesis of methionine from homocysteine. Wild type carries out all essen- 

 tial reactions and produces all essential growth factors, with the exception 

 of biotin which must be supplied to all strains. 



The reaction governed by the sulfonamide-requiring gene has not yet been 

 identified, but we know quite a little about it. It requires the presence of both 

 homocysteine and />-aminobenzoic acid. Presumably homocysteine is used as 

 a substrate in this reaction, and />-aminobenzoic acid, or a derivative, is 

 needed as a catalyst. The reaction either results in the destruction of threo- 

 nine or else interferes with its normal utilization, so that the sulfonamide- 

 requiring strain has too little threonine for growth. W^e also know that more 

 homocysteine is required for this deleterious reaction than for the syn- 

 thesis of methionine, and that in the presence of limiting amounts of homo- 

 cysteine, the synthesis of methionine goes on without any interference with 

 the utilization of threonine. 



Furthermore, the deleterious reaction requires larger amounts of ^-amino- 

 benzoic acid than are needed for all essential reactions combined. Only about 

 half as much is needed in the synthesis of methionine, about a quarter as 

 much in the production of purines, and very much less still for other essen- 

 tial, but still unidentified factors. Both wild type and the sulfonamide-requir- 

 ing strain produce about one hundred times as much />-aminobenzoic acid as 

 is needed for all essential reactions. 



We know of three ways in which the deleterious reaction leading to threo- 



